An isolated cardiac muscle cell, beating

Cardiac muscle (heart muscle) is involuntary striated muscle that is found in the walls and histological foundation of the heart, specifically the myocardium. Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle. These three types of muscle all form in the process of myogenesis. The cells that constitute cardiac muscle, called cardiomyocytes or myocardiocytes, contain only three nuclei.[1][2][pageneeded] The myocardium is the muscle tissue of the heart, and forms a thick middle layer between the outer epicardium layer and the inner endocardium layer.

Coordinated contractions of cardiac muscle cells in the heart propel blood out of the atria and ventricles to the blood vessels of the left/body/systemic and right/lungs/pulmonary circulatory systems. This complex mechanism illustrates systole of the heart.

Cardiac muscle cells, unlike most other tissues in the body, rely on an available blood and electrical supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide. The coronary arteries help fulfill this function.

Cardiac muscle has cross striations formed by rotating segments of thick and thin protein filaments. Like skeletal muscle, the primary structural proteins of cardiac muscle are myosin and actin. The actin filaments are thin, causing the lighter appearance of the I bands in striated muscle, whereas the myosin filament is thicker, lending a darker appearance to the alternating A bands as observed with electron microscopy. However, in contrast to skeletal muscle, cardiac muscle cells are typically branch-like instead of linear.

Another histological difference between cardiac muscle and skeletal muscle is that the T-tubules in the cardiac muscle are bigger and wider and track laterally to the Z-discs. There are fewer T-tubules in comparison with skeletal muscle. The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single T-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca2+ ions. This way, the wave of depolarization can be coupled to calcium-mediated cardiac muscle contraction via the sliding filament mechanism. Cardiac muscle forms these instead of the triads formed between the sarcoplasmic reticulum in skeletal muscle and T-tubules. T-tubules play critical role in excitation-contraction coupling (ECC). Recently, the action potentials of T-tubules were recorded optically by Guixue Bu et al.[3]

The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres.[4] Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncyntium obeys the all or none law.[5]

Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development). The discs are responsible mainly for force transmission during muscle contraction. Intercalated discs are described to consist of three different types of cell-cell junctions: the actin filament anchoring adherens junctions, the intermediate filament anchoring desmosomes , and gap junctions. They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. However, novel molecular biological and comprehensive studies unequivocally showed that intercalated discs consist for the most part of mixed-type adhering junctions named area composita (pl. areae compositae) representing an amalgamation of typical desmosomal and fascia adhaerens proteins (in contrast to various epithelia).[6][7][8] The authors discuss the high importance of these findings for the understanding of inherited cardiomyopathies (such as arrhythmogenic right ventricular cardiomyopathy).

Under light microscopy, intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section.[9]

In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which allows myosin to bind to actin and contraction to occur.

Until recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief.[10] Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 20-year-old renews about 1% of heart muscle cells per year, and about 45 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.

One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process.[11] The division process of pre-existing cardiomyocytes has also been shown to increase in areas adjacent to sites of myocardial injury. In addition, certain growth factors promote the self-renewal of endogenous cardiomyocytes and cardiac stem cells. For example, insulin-like growth factor 1, hepatocyte growth factor, and high-mobility group protein B1 increase cardiac stem cell migration to the affected area, as well as the proliferation and survival of these cells.[12] Some members of the fibroblast growth factor family also induce cell-cycle re-entry of small cardiomyocytes. Vascular endothelial growth factor also plays an important role in the recruitment of native cardiac cells to an infarct site in addition to its angiogenic effect.

Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce regeneration of damaged tissue. Various stem cell lineages have been shown to be able to differentiate into cardiomyocytes, including bone marrow stem cells. For example, in one study, researchers transplanted bone marrow cells, which included a population of stem cells, adjacent to an infarct site in a mouse model. Nine days after surgery, the researchers found a new band of regenerating myocardium.[13] However, this regeneration was not observed when the injected population of cells was devoid of stem cells, which strongly suggests that it was the stem cell population that contributed to the myocardium regeneration. Other clinical trials have shown that autologous bone marrow cell transplants delivered via the infarct-related artery decreases the infarct area compared to patients not given the cell therapy.[14]

Occlusion (blockage) of the coronary arteries by atherosclerosis and/or thrombosis can lead to myocardial infarction (heart attack), where part of the myocardium is injured due to ischemia (not receiving enough oxygen). This occurs because coronary arteries are functional end arteries - i.e. there is almost no overlap in the areas supplied by different arteries (anastomoses) so that if one fails, others cannot adequately perfuse the region, unlike in other tissues.

Certain viruses lead to myocarditis (inflammation of the myocardium). Cardiomyopathies are inherent diseases of the myocardium, many of which are caused by genetic mutations.

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Cardiac muscle - Wikipedia, the free encyclopedia

George Reed's heart wasn't doing so well: He's 71, and after suffering a heart attack years earlier, Reed had undergone open heart surgery and was put on multiple medications. But nothing seemed to help the dizziness and chest pain he experienced daily.

"I'd get dizzy and just fall over -- sometimes twice a day. I would run my head into the concrete. I was a bloody mess," the Perry, Ohio, native says. Despite his doctor's best efforts, Reed continued to experience angina, a type of chest pain that occurs when the heart doesn't get enough oxygen-rich blood; it can be accompanied by dizziness. So when he was recommended for an experimental study that would inject his own stem cells into his damaged heart, Perry signed on. "I needed something to change," he says.

Researchers gave Reed a drug commonly used in bone marrow transplants that stimulates the marrow to make more stem cells. Then they removed some of Reed's blood, isolated the stem cells and injected them into and around the damaged areas of his heart.

"The goal was to grow new blood vessels with stem cells from the patient's own body," says Dr. Tim Henry, a co-author of the study and director of research at the Minneapolis Heart Institute Foundation.

Within a few months, Reed, along with many of the other 100 or so patients at 26 hospital centers who'd received this stem cell treatment, reported feeling better than he had in years.

"When it started kicking in, I felt like a kid. I felt good," Reed says. He wasn't passing out and falling down anymore.

For Jay Homstad, 49, who was part of the Minnesota branch of the study, he felt the changes most in his ability to walk and be active.

"My activity level increased tenfold. Before, I struggled with chest pain every day. My activity level was about as close to zero as you could get. Now I can participate ... just in life. It may sound silly, but the best part is that in the wintertime I could go out and walk with my dog along the Red River. When you're walking through snow that is waist deep, you can tell there's a difference," Homstad says.

Homstad had had about a dozen surgeries and nine stents put in before he enrolled in the study, but he still struggled with angina daily. Within a few months of the stem cell shots, he could walk farther, and his chest pain subsided and was kept at bay for nearly four years.

"These are people for whom other treatment hasn't worked. They're debilitated by their chest pain, but their other options are really limited, that's why we picked them," says Henry. If the positive results seen in this study hold up in the next phase of the study, which is set to begin enrollment in the fall, this type of cardiac stem cell injection could be added to the arsenal of weapons against angina. The upcoming phase three trial has already been approved by the Food and Drug Administration.

Shot to the Heart, Before It's too Late

While several smaller studies have suggested that injecting stem cells into damaged heart tissue might be effective, this study, in its scope and rigor, was the first of its kind. A total of 167 patients were recruited and randomly assigned to receive a lower dose of stem cells, a higher dose or a placebo. The patients didn't know who got what treatment, and neither did the doctors treating them.

When tracked for a year after the injection, patients who received the lower dose of stem cells could last longer during a treadmill exercise than those who had received the placebo, and they averaged seven fewer episodes of chest pain in a week. To put this in perspective, a popular drug to treat angina, Ranolazine, reduced chest pain by fewer than two episodes a week in clinical trials.

Although the goal of the stem cell shots was to grow new blood vessels, it's impossible to tell if these stem cells were actually growing into blood vessels or if they were just triggering some other kind of healing process in the body, Henry says. Tests in animal models, however, do suggest that new blood vessels are forming, says Dr. Marco Costa, a co-author of the study and George Reed's doctor at UH Case Medical Center in Cleveland.

For now, the only gauge of the injections is improvement in symptoms.

Despite the positive results of the study, cardiologists remain "cautiously optimistic" about stem cells as a treatment for angina.

"The number of patients is relatively small, so this trial would probably not carry much scientific weight," says Dr. Jeff Brinker, a professor of cardiology at Johns Hopkins University. The results did justify the next, larger trial, he says, which would offer more answers as to whether this treatment is actually working the way researchers suspect.

The fact that lower doses of stem cells were puzzlingly more effective than larger ones is cause for caution, says Dr. Steve Nissen, chairman of the department of cardiovascular medicine at the Cleveland Clinic.

"The jury is still out for stem cell therapies to treat heart disease," says Dr. Cam Paterson, a cardiologist at the University of North Carolina at Chapel Hill.

But the results so far provide cautious hope for heart patients like George Reed and Jay Homstad.

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Injecting the Heart With Stem Cells Helps Chest Pain - ABC ...

Stem Cell Therapy: Helping the Body Heal Itself

Stem cells are natures own transformers. When the body is injured, stem cells travel the scene of the accident. Some come from the bone marrow, a modest number of others, from the heart itself. Additionally, theyre not all the same. There, they may help heal damaged tissue. They do this by secreting local hormones to rescue damaged heart cells and occasionally turning into heart muscle cells themselves. Stem cells do a fairly good job. But they could do better for some reason, the heart stops signaling for heart cells after only a week or so after the damage has occurred, leaving the repair job mostly undone. The partially repaired tissue becomes a burden to the heart, forcing it to work harder and less efficiently, leading to heart failure.

Initial research used a patients own stem cells, derived from the bone marrow, mainly because they were readily available and had worked in animal studies. Careful study revealed only a very modest benefit, so researchers have moved on to evaluate more promising approaches, including:

No matter what you may read, stem cell therapy for damaged hearts has yet to be proven fully safe and beneficial. It is important to know that many patients are not receiving the most current and optimal therapies available for their heart failure. If you have heart failure, and wondering about treatment options, an evaluation or a second opinion at a Center of Excellence can be worthwhile.

Randomized clinical trials evaluating these different approaches typically allow enrollment of only a few patients from each hospital, and hence what may be available at the Cleveland Clinic varies from time to time. To inquire about current trials, please call 866-289-6911 and speak to our Resource Nurses.

Cleveland Clinic is a large referral center for advanced heart disease and heart failure we offer a wide range of therapies including medications, devices and surgery. Patients will be evaluated for the treatments that best address their condition. Whether patients meet the criteria for stem cell therapy or not, they will be offered the most advanced array of treatment options.

Allogenic: from one person to another (for example: organ transplant)

Autogenic: use of one's own tissue

Myoblasts: immature muscle cells, may be able to change into functioning heart muscle cells

Stem Cells: cells that have the ability to reproduce, generate new cells, and send signals to promote healing

Transgenic: Use of tissue from another species. (for example: some heart valves from porcine or bovine tissue)

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Stem Cell Therapy for Heart Disease - Cleveland Clinic

A new method for delivering stem cells to damaged heart muscle has shown early promise in treating severe heart failure, researchers report.

In a preliminary study, they found the tactic was safe and feasible for the 48 heart failure patients they treated. And after a year, the patients showed a modest improvement in the heart's pumping ability, on average.

It's not clear yet whether those improvements could be meaningful, said lead researcher Dr. Amit Patel, director of cardiovascular regenerative medicine at the University of Utah.

He said larger clinical trials are underway to see whether the approach could be an option for advanced heart failure.

Other experts stressed the bigger picture: Researchers have long studied stem cells as a potential therapy for heart failure -- with limited success so far.

"There's been a lot of promise, but not much of a clinical benefit yet," said Dr. Lee Goldberg, who specializes in treating heart failure at the University of Pennsylvania.

Researchers are still sorting through complicated questions, including how to best get stem cells to damaged heart muscle, said Goldberg, who was not involved in the new study.

What's "novel" in this research, he said, is the technique Patel's team used to deliver stem cells to the heart. They took stem cells from patients' bone marrow and infused them into the heart through a large vein called the coronary sinus.

Patel agreed that the technique is the advance.

"Most other techniques have infused stem cells through the arteries," Patel explained. One obstacle, he said, is that people with heart failure generally have hardened, narrowed coronary arteries, and the infused stem cells "don't always go to where they should."

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Stem Cells Show Promise in Heart Failure Treatment

Clara's Story

Clara had a severe heart attack in 2004. Before contacting us she had received adult stem cells from a company in Thailand - a process requiring at least a one week stay.

When she contacted Stemaid, she had just had an echocardiogram showing that her overall left ventricular ejection fraction was estimated to be 30 to 35%. She opted to receive one injection of 5 million Embryonic Stem Cells by Stemaid in November 2010. She arrived at 1pm and was done by 3pm the same day.

We received the following email from her in April 2011: I had an EKO last week and rate is 44%, up from the 33/35% it was before I received Stemaid's stem cells! . Are the stem cells still available and still as good?

The heart contains a small amount of stem cells, the cardiac stem cells, that are produced when there is a need for production of more heart cells or for an active replacement of damaged ones. These cardiac cells are produced in high quantity for about one week following an infarction, actively repairing the damaged areas of the heart.

However this high production stops after a week and the repair stops as well.

Initial studies showed that by introducing embryonic stem cells, the heart starts to repair again within minutes of their injection. More recent studies showed that the injection of embryonic stem cells actually triggers the production of cardiac stem cells for one week. Another week of active repair is offered each time that one receives embryonic stem cells.

If you have suffered from an infarction, we suggest a minimum of 3 injections of esc over the course of 3 weeks to get significant repair.

Some of the patients who have received Stemaid Embryonic Stem-Cells have agreed to be mentioned on our website so that we may illustrate the benefits of them.

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Heart Disease - Stemaid : Embryonic Stem-cells

Stem Cell Clinical Research & Deployment Cardiovascular & Pulmonary Conditions

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use ofAdult Autologous Adipose-derived Stem Cells (ADSCs) for clinical research and deployment for numerous Cardiovascular and Pulmonary disorders, inclusive of:

Cardiovascular conditions include medical problems involving the heart and vascular system (the arterial and venous blood vessels). The most common cardiovascular condition is atherosclerotic coronary artery disease (ASCVD), which especially affects the coronary arteries and is the leading cause of heart attacks and death worldwide; and Congestive Heart Failure (CHF).

Other common cardiovascular conditions involve the cardiac muscle (CHF), cardiac valves, and heart rhythm. Many patients are typically treated with a multitude of medications; many patients require surgical interventions such as coronary angioplasty, coronary artery bypass, or other surgeries. Often patients, despite maximum therapy with medications and surgery, continue to suffer pain, discomfort, disability and have marked restrictions in their normal daily living activities.

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. We have an array of ongoing IRB-approved protocols, andwe provide care for patients with a wide variety of disorders that may be treated with adult stem cell-based regenerative therapy.

The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use of Autologous Adult Adipose Derived Stem Cells (ADSCs) for clinical research and deployment for numerous cardiovascular conditions. These ADSCs cells are derived from fat an exceptionally abundant source of stem cells that has been removed during our mini-liposuction office procedure. The source of the regenerative stem cells actually comes from stromal vascular fraction (SVF) a protein rich segment from processed adipose tissue. SVF contains a mononuclear cell line (predominantly autologous mesenchymal stem cells), macrophage cells, endothelial cells, red blood cells, and important growth factors that facilitate the stem cell process and promote their activity. Our technology allows us to isolate high numbers of viable cells that we can deploy during the same surgical setting.

The SVF and stem cells are then deployed back into the patients body via injection or IV infusion on an outpatient basis; the total procedure takes less than two hours; and only local anesthesia is used. Not all cardiovascular problems respond to stem cell therapy, and each patient must be assessed individually to determine the potential for optimal results from this regenerative medicine process.

The Manhattan Regenerative Medicine Medical Group is committed not only to providing a high degree of quality care for our patients with cardiovascular problems but we are also highly committed to clinical stem cell research and the advancement of regenerative medicine. At the Miami Stem Cell Treatment Center we exploit anti-inflammatory, immuno-modulatory and regenerative properties of adult stem cells to mitigate cardiovascular conditions which are otherwise lethal to our bodies.

Myocardial infarction (heart attack) is responsible for significant cardiac muscle destruction and impairment due to ischemia (lack of blood flow). This can lead to further or recurrent restriction of blood flow thereby causing re-current infarct and pain on exertion (or even rest) known as chronic angina. Chronic angina causes restriction of daily activities of everyday living and is plagued with chest pain, chest pressure, and depression. This problem is caused most commonly by coronary artery disease which is very common in the United States and associated with significant morbidity and mortality.

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Cardiovascular Stem Cell Therapy

Abstract

Myocardial infarctioninduced heart failure is a prevailing cause of death in the United States and most developed countries. The cardiac tissue has extremely limited regenerative potential, and heart transplantation for reconstituting the function of damaged heart is severely hindered mainly due to the scarcity of donor organs. To that end, stem cells with their extensive proliferative capacity and their ability to differentiate toward functional cardiomyocytes may serve as a renewable cellular source for repairing the damaged myocardium. Here, we review recent studies regarding the cardiogenic potential of adult progenitor cells and embryonic stem cells. Although large strides have been made toward the engineering of cardiac tissues using stem cells, important issues remain to be addressed to enable the translation of such technologies to the clinical setting.

Heart disease is a significant cause of morbidity and mortality worldwide. In the United States, heart failure is ranked number one as a cause of death, affecting over 5 million people and with more than 500,000 new cases diagnosed each year.1 The health care expenditures associated with heart failure were $26.7 billion in 2004 and are estimated to $33.2 billion in 2007. Although significant progress has been made in mechanical devices and pharmacological interventions, more than half of the patients with heart failure die within 5 years of initial diagnosis. Wide application of heart transplantation is severely hindered by the limited availability of donor organs. To this end, cardiac cell therapy may be an appealing alternative to current treatments for heart failure.

Recent investigations focusing on engineering cells and tissues to repair or regenerate damaged hearts in animal models and in clinical trials have yielded promising results. Considering the limited regenerative capacity of the heart muscle, renewable sources of cardiomyocytes are highly sought. Cells suitable for myocardial engineering should be nonimmunogenic, should be easy to expand to large quantities, and should differentiate into mature, fully functional cardiomyocytes capable of integrating to the host tissue. Adult progenitor cells (APCs) and embryonic stem cells (ESCs) have extensive proliferative potential and can adopt different cell fates, including that of heart cells. The recent advances in the fields of stem cell biology and heart tissue engineering have intensified efforts toward the development of regenerative cardiac therapies. In this article, we review findings pertaining to the cardiogenic potential of major APC populations and of ESCs (). We also discuss significant challenges in the way of realizing stem cellbased therapies aiming to reconstitute the normal function of heart.

Potential sources of stem/progenitor cells for cardiac repair. ESCs derived from the inner cell mass of a blastocyst can be manipulated ex vivo to differentiate toward heart cells. APCs residing in various tissues such as the BM and skeletal muscle may ...

Bone marrow (BM) is a heterogeneous tissue comprising of multiple cell types, including minute fractions of mesenchymal stem cells (MSCs; 0.0010.01% of total cells2) and hematopoietic stem cells (HSCs; 0.71.5cells/108 nucleated marrow cells3). The heterogeneity of BM makes challenging the identification of a subpopulation of cells capable of cardiogenesis, and studies of BM celltocardiac cell transdifferentiation should be examined through this prism.

The notion that BM-derived cells may contribute to the regeneration of the heart was first illustrated when dystrophic (mdx) female mice received BM cells from male wild-type mice.4 More than 2 months after the transplantation, tissues of the recipient mice were histologically examined for the presence of Y-chromosome+ donor cells. Besides the skeletal muscle, donor cells were identified in the cardiac region, suggesting that circulating BM cells contribute to the regeneration of cardiomyocytes.

Further supporting evidence was provided by Jackson et al.5 in studies using a side population (SP) of cells characterized by their intrinsic capacity to efflux Hoechst 33342 dye through the ATP-binding Bcrp1/ABCG2 transporter. The cells were isolated from the BM fraction of HSCs of Rosa26 mice constitutively expressing the -galactosidase reporter gene (LacZ). After SP cells were injected into mice with coronary occlusioninduced ischemia, cells coexpressing LacZ and cardiac -actinin were identified around the infarct region with a frequency of 0.02%. Endothelial engraftment was more prevalent (3.3%). The observed improvement in myocardial function may thus be attributed to the potential of BM cells to give rise to a rather endothelial progeny. This may be a parallel to cardiovascular progenitors from differentiating ESCs giving rise to cardiomyocytes, and endothelial and vascular smooth muscle lineages.6,7

Orlic et al.8 also reported the regeneration of infarcted myocardium after transplantation of lineage-negative (LIN)/C-KIT+ BM cells from transgenic mice constitutively expressing enhanced green fluorescent protein (eGFP). Cells were injected in the contracting wall close to the infarct area. Nine days after transplantation, an impressive 68% of the infarct was occupied by newly formed myocardium with eGFP+ cells displaying cardiomyocyte markers such as troponin, MEF2, NKX2.5, cardiac myosin, GATA-4, and -sarcomeric actin. Similar outcomes were reported by the same group9 when mouse C-KIT+ (but not screened for LIN) BM cells were transplanted.

Although these findings led to the conclusion that BM cells can repopulate a damaged heart, work by other investigators has casted doubt on this assertion. Balsam et al.10 noted that mice with infarcts receiving BM LIN/C-KIT+, C-KIT-enriched or THY1.1low/LIN/stem cell antigen-1 (SCA-1+) cells exhibited improved ventricular function. However, donor cells expressed granulocyte but not heart cell markers 1 month after injection. In another study,11 HSCs carrying a nuclear-localized LacZ gene flanked by the cardiac -myosin heavy chain promoter were delivered into the periinfarct zone of mice 5h after coronary artery occlusion. One to 4 weeks later, LacZ+ cells were absent in heart tissue sections from 117 mice that received HSCs. Similarly, no eGFP+ cells were detected in the infarcted hearts of mice infused with BM cells constitutively expressing eGFP. Finally, Nygren et al.12 in similar transplantation experiments observed only blood cells (mainly leukocytes) originating from BM HSCs in the infarcted myocardium without evidence of transdifferentiation of donor cells to cardiomyocytes.

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Stem Cells for Heart Cell Therapies - National Center for ...

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

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cardiovascular disease :: Cardiac stem cells | Britannica.com

Tsai et al./Stem Cell Reports 2015

Weill Cornell investigators have discovered how to generate large numbers of rare cells in the network that pushes the heart's chambers to consistently contract. In this image, investigators stained these cells, generated from embryonic stem cells, to reveal cell-specific genes (green and red, indicated by arrows). The blue represents stained cell nuclei.

For the first time, scientists can efficiently generate large numbers of rare cells in the network that pushes the heart's chambers to consistently contract. The technique, published May 28 in Stem Cell Reports, could be a first step toward using a person's own cells to repair an irregular heartbeat known as cardiac arrhythmia.

This study, while done using mouse cells, will now allow us to develop human heart cells and test their function in repairing damaged hearts, said the study's senior author, Dr. Todd Evans, vice chair for research and the Peter I. Pressman Professor in the Department of Surgery at Weill Cornell Medical College.

The human heart beats billions of times during a lifetime, so it's not surprising that development of irregular heartbeats can lead to a variety of cardiac diseases, Evans says. But treatments for these disorders are costly, and often ineffective.

The government pays more than $3 billion each year for cardiac arrhythmia-related diseases. Despite this enormous expense, the treatments we have available are inadequate, Evans said. For example, artificial pacemakers are often used, but these can fail, and are particularly challenging therapies for children.

One solution is to coax a patient's own cells to generate the specific kinds of cells in the cardiac conduction system (CCS) that maintain a regular heartbeat.

We can imagine someday using these cells, for example, to create patches that can replace defective conduction fibers. Of course this is still a long way off, as we would need to study how to coax them into integrating properly with the rest of the CCS, Evans said. But previously, we did not even have the capacity to generate the cells, and now we can do so in a manner that is scalable, so that such preclinical research is now feasible.

Evans worked with Dr. Shuibing Chen, an expert in stem cell and chemical biology, and Dr. Su-Yi Tsai, a postdoctoral fellow and the study's lead investigator. Other key contributors were from the laboratory of Dr. Glenn Fishman, who specializes in cardiac physiology at New York University.

Their first goal was to increase the efficiency of coaxing mouse embryonic stem cells to become CCS cells. They created mouse stem cells that can express a CCS marker gene that can be quantified. This allows them to measure how many embryonic cells morph into CCS cells.

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Stem cell technology could lead to ailing heart mending ...

Dr. Gabriele DUva is finishing up his postdoctoral research at the Weizmann Institute. Here is his account of three years of highly successful research on regenerating heart cells after injury. Among other things, it is the story of the way that different ideas from vastly different research areas can, over the dinner table or in casual conversation, provide the inspiration for outstanding research:

Three years ago, when I joined the lab of Prof. Eldad Tzahor, the emerging field of cardiac regeneration was totally obscure to me. My scientific track at that time was mainly focused on normal and cancer stem cells: cells that build our bodies during development and adulthood. The deregulation of these cells can lead to cancer. I have to admit that I didnt know even the shape of a cardiac cell when my postdoc journey started

Eldads lab was also switching fields well, not drastically, like me, but still it was a transition from a basic research on the development of the heart to the challenge of heart regeneration during adult life.

Two neonatal cardiomyocytes (staining in red) undergoing cell division after treatment with NRG1

In contrast to most tissues in our body, which renew themselves throughout life using our pools of stem cells, the renewal of heart cells in adulthood is extremely low; it almost doesnt exist. Just to give an approximate picture of renewal and regeneration processes: Every day we produce billions of new blood cells that completely replace the old ones in a few months. In contrast, heart cells renewal is so low that, many cardiac cells remain with us for our entire life, from birth to death! Consequently, heart injuries cannot be truly repaired, leading to (often lethal) cardiovascular diseases. This might appear somewhat nonsensical, since the heart is our most vital organ: No (heart) beat no life.

Hence a challenge for many scientists is to understand how to induce heart regeneration Scientists have been trying different strategies, for example, the injection of stem cells. We decided to adopt a different strategy one that mimics the natural regenerative process of healing the heart in such regenerative organisms as amphibians and fish, and even newly-born mice. In all these cases the regeneration of the heart involves the proliferation of heart muscle cells called cardiomyocytes. Therefore the challenge before us was: How can we push cardiomyocytes to divide?

We adopted a team strategy. Cancer turned out to be a somewhat useful model for a strategy. After all, the hallmark of this disease is continuous self-renewal and cell proliferation. Starting from this thought, Prof. Yossi Yarden, a leading expert in the cancer field, suggested: Why dont you try an oncogene, such as ERBB2, whose deregulation can lead to uncontrolled cellular growth and tumour development? The idea was that cardiomyocytes could be pushed into a proliferative state by this cancer-promoting agent. To Eldad, this was a nice life circle closing, since Eldad, when he was a PhD student in Yossis lab, focused exactly on the ERBB2 mechanism of action in cancer progression. I must admit, the idea sounded very intriguing and I really liked it.

Eldad, as a developmental biologist, had a different approach. Based on his field of expertise, his tactic was to apply proliferative (and regenerative) strategies learned from the embryos, when heart cells normally proliferate to form a functional organ. It turned out that a key player in driving embryonic heart growth is again ERBB2!

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Guest post: Dr. Gabriele DUva: How to Grow New Heart Cells [The Weizmann Wave]

Welcome

The Stem Cell Center Texas Heart Institute is dedicated to the study of adult stem cells and their role in treating diseases of the heart and the circulatory system. Through numerous clinical and preclinical studies, we have come to realize the potential of stem cells to help patients suffering from cardiovascular disease.We are actively enrolling patients in studies using stem cells for the treatment of heart failure, heart attacks, and peripheral vascular disease.

Whether you are a patient looking for information regarding our research, or a doctor hoping to learn more about stem cell therapy, we welcome you to the Stem Cell Center. Please visit our Clinical Trials page for more information about our current trials.

Emerson C. Perin, MD, PhD, FACC Director, Clinical Research for Cardiovascular Medicine Medical Director, Stem Cell Center McNair Scholar

You may contact us at:

E-mail: stemcell@texasheart.org Toll free: 1-866-924-STEM (7836) Phone: 832-355-9405 Fax: 832-355-9440

We are a network of physicians, scientists, and support staff dedicatedto studying stem cell therapy for treating heart disease. Thegoals of the Network are to complete research studies that will potentially lead to more effective treatments for patients with cardiovasculardisease, and to share knowledge quickly with the healthcare community.

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The Stem Cell Center at Texas Heart Institute

For millions of people around the world, who suffer from various diseases, research in stem cells offers a ray of hope. Scientists of the city-based Indian Institute of Science have used stem cells of a mouse to culture cardiac cells.

Explaining the research, Polani B. Seshagiri said their research over the past seven years has helped develop cardiac cells that function and beat in rhythms identical to the original cell.

Speaking on Stem Cell Awareness Day recently, Prof. Seshagiri said stem cells had several advantages and could cure human disorders and diseases, which could not be cured by conventional approaches. However, he warned that there was a need to be aware of the limitations of stem cells.

Sudarshan Ballal, Medical Director, Manipal Health Enterprise, said stem cells had enormous potential as they never die and could be converted into any cell. Stem cells can be converted into organs and maybe years later, organs can be cultivated in labs through stem cell, he said. Elaborating further, he said a stem cell could be compared to a bicycle, which could turn into car, motorbike and spaceship based on the environment and conditions.

Nazeer Ahmed, Deputy Drug Controller of Karnataka, said they were in the process of chalking out regulations for stem cells as there were currently no rules to regulate stem cell research and therapy.

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Scientists develop cardiac cells using stem cells

for the first time, scientists - including an Indian American bioengineer - have developed a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue.

This organ-on-a-chip represents a major step forward in the development of accurate, faster methods of testing for drug toxicity.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said professor Kevin Healy of University of California, Berkeley, who led the team.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral scholar in Healy's lab.

"We designed this system so that it is dynamic. It replicates how tissue in our bodies actually gets exposed to nutrients and drugs," Mathur explained.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs.

Much of the failure is due to fundamental differences in biology between species, the researchers explained.

"Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market," Healy added.

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3D structure would be comparable to the geometry and spacing of connective tissue fibre in a human heart.

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Human 'heart on a chip' to aid drug tests

CIRM funds many projects seeking to better understand heart disease and to translate those discoveries into new therapies.

If you want to learn more about CIRM funding decisions or make a comment directly to our board, join us at a public meeting. You can find agendas for upcoming public meetings on our meetings page.

Find Out More: Stem Cell FAQ | Stem Cell Videos | What We Fund

Find clinical trials: CIRM does not track stem cell clinical trials. If you or a family member is interested in participating in a clinical trial, please visit clinicaltrials.gov to find a trial near you.

Heart disease strikes in many forms, but collectively it causes one third of all deaths in the U.S. Many forms of heart disease have a common resultcardiomyopathy. While this is commonly called congestive heart failure (CHF), it is really just the heart becoming less efficient due to any number of causes, but the most common is loss of functioning heart muscle due to the damage caused by a heart attack. An estimated 4.8 million Americans have CHF, with 400,000 new cases diagnosed each year. Half die within five years.

Numerous clinical trials are underway testing a type of stem cell found in borne marrow, called mesenchymal stem cells or MSCs, to see if they are effective in treating the form of CHF that follows a heart attack. While those trials have shown some small improvements in patients the researchers have not found that the MSCs are creating replacement heart muscle. They think the improvements may be due to the MSCs creating new blood vessels that then help make the existing heart muscle healthier, or in other ways strengthening the existing tissue.

Californias stem cell agency has numerous awards looking into heart disease (the full list is below). Most of these involve looking for ways to create stem cells that can replace the damaged heart muscle, restoring the hearts ability to efficiently pump blood around the body. Some researchers are looking to go beyond transplanting cells into the heart and are instead exploring the use of tissue engineering technologies, such as building artificial scaffolds in the lab and loading them with stem cells that, when placed in the heart, may stimulate the recovery of the muscle.

Other CIRM-funded researchers are working in the laboratory, looking at stem cells from heart disease patients to better understand the disease and even using those models to discover and test new drugs to see if they are effective in treating heart disease. Other researchers are trying to make a type of specialized heart cell called a pacemaker cell, which helps keep a proper rhythm to the hearts beat.

We also fund projects that are trying to take promising therapies out of the laboratory and closer to being tested in people. These Disease Team Awards encourage the creation of teams that have both the scientific knowledge and business skills needed to produce therapies that can get approval from the Food and Drug Administration (FDA) to be tested in people. In some cases, these awards also fund the early phase clinical trials to show that they are safe to use and, in some cases, show some signs of being effective.

This team developed a way to isolate some heart-specific stem cells that are found in adult heart muscle. They use clumps of cells called Cardiospheres to reduce scarring caused by heart attacks. Initially they used cells obtained from the patients own heart but they later developed methods to obtain the cells they need from donor organs, which allows the procedure to become an off-the-shelf-therapy, meaning it can be available when and where the patient needs it rather than having to create it new each time. The company, working with the Cedars-Sinai team, received FDA approval to begin a clinical trial in June 2012.

Read the rest here:
Heart Disease Fact Sheet | California's Stem Cell Agency

CardioCel has been initially well received with surgeons in Australia and overseas. Photo: Geoff Fisher

For 10 years researchers at Admedus worked day and night trying to work out how to improve soft tissue repair in the human body.

And with the vital help of CSIRO they have been to develop CardioCel, a life-saving heart patch for the repair and reconstruction of cardiovascular defects.

According to the Children's Heart Foundation, congenital heart disease occurs in one out of 100 births and in at least half of those cases surgery is required and a patch is needed. They state it is the leading cause of birth defect related deaths.

Research undertaken with CSIRO investigated new, potentially ground-breaking applications for CardioCel. The research focused on using stem cells. It found the heart patch has the potential to deliver stem cells and help tissue heal better than other existing products, when used for cardiac repair.

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Derived from animal tissue, the CardioCel patch is engineered over 14 days.

"The first unique feature of this product is that it doesn't calcify in young patients," Professor Leon Neethling, Admedus technical director and heart researcher says.

The flexible patch works like human tissue to cover holes in the heart thereby eliminating the need for repeat surgery.

"In the cardiac repair field it has long been recognised that strong, flexible, biocompatible and calcification-resistant tissue scaffolds would be ideal tissues for repair of heart defects," Admedus' chief operating officer Dr Julian Chick, says.

The rest is here:
Local innovation repairs holes in the heart

Newport Beach, California (PRWEB) March 31, 2015

Newport Beach based charity Coalition Duchenne has launched an interview series titled Making a Difference in Duchenne on its Youtube channel (https://www.youtube.com/user/CoalitionDuchenne) focused on individuals making a difference in Duchenne muscular dystrophy research, care, awareness, and education.

The first interview features Dr. Eduardo Marbn MD, PhD, director of the Cedars-Sinai Heart Institute in Los Angeles, talking about cardiac derived stem cells. Dr. Marbn was featured in a November 2011 Economist article Repairing Broken Hearts, read by Coalition Duchenne founder and executive director Catherine Jayasuriya. She lobbied for a focus on Duchenne because cardiac scarring severely compromises the life span of those with the disease. Coalition Duchenne funded successful research applying Marbns stem cell technology to Duchenne. The approach has been clinically proven to mitigate scarring cause by heart attacks. In Marbns therapy, human heart tissue is used to grow specialized heart stem cells, which are injected back into the patients heart.

We need to focus on changing the course of the disease. We lose many young men to cardiac issues. We hope that working with cardiac stem cells is one way we will eventually change that outcome, said Jayasuriya.

The second interview in the Making a Difference in Duchenne series features actor Cody Saintgnue, who plays Brett Talbot in MTVs Teen Wolf. Saintgnue has a unique relationship with Duchenne. He played a young man with muscular dystrophy in his break out role on House MD in 2009. Saintgnue talks about his experience learning to mimic the physicality of a young man with Duchenne, as well as the inspiration he draws from the way those young men overcome many obstacles to live happy, fulfilling lives.

Upcoming interviews will feature: Professor Rachelle Crosbie-Watson from the University of California, Los Angeles, who teaches the first university course focused entirely on Duchenne; Dr. Ron Victor, a Cedars-Sinai cardiologist and researcher looking at the benefits of Cialis and Viagra for Duchenne cardiomyopathy; and, Scotty Bob Morgan, a daredevil wingsuit pilot, who has raised awareness worldwide about Duchenne, flying a specially made Coalition Duchenne wingsuit.

About Duchenne muscular dystrophy: Duchenne muscular dystrophy is a progressive muscle wasting disease. It is the most common fatal disease that affects children. Duchenne occurs in 1 in 3,500 male births, across all races, cultures and countries. Duchenne is caused by a defect in the gene that codes for the protein dystrophin. This is a vital protein that helps connect the muscle fiber to the cell membranes. Without dystrophin, the muscle cells become unstable, are weakened and lose their functionality. Life expectancy ranges from the mid teenage years to the mid 20s. Their minds are unaffected.

About Coalition Duchenne: Jayasuriya founded Coalition Duchenne in 2010 (http://www.coalitionduchenne.org) to raise global awareness for Duchenne muscular dystrophy, to fund research and to find a cure for Duchenne. Coalition Duchenne is a 501c3 non-profit corporation.

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Coalition Duchenne Launches Youtube Interview Series 'Making a Difference in Duchenne'

The growing number of biological structures being grown on chips in various laboratories around the world is rapidly replicating the entire gamut of major human organs. Now one of the most important of all a viable functioning heart has been added to that list by researchers at the University of California at Berkeley (UC Berkeley) who have taken adult stem cells and grown a lattice of pulsing human heart tissue on a silicon device.

Sourced from human-induced pluripotent stem cells able to be persuaded into forming many different types of tissue, the human heart device cells are not simply separate groups of cells existing in a petri dish, but a connected series of living cells molded into a structure that is able to beat and react just like the real thing.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral researcher at UC Berkeley. "We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

Touted as a possible replacement for living animal hearts in drug-safety screening, the ability to easily access and rapidly analyze a heart equivalent in experiments presents appealing advantages.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said professor of bioengineering at UC Berkeley, and leader of the research team, Kevin Healy.

The cardiac microphysiological system, as the team calls its heart-on-a-chip, has been designed so that its silicon support structure is equivalent to the arrangement and positioning of conjoining tissue filaments in a human heart. To this supporting arrangement, the researchers loaded the engineered human heart cells into the priming tube, whose cone-shaped funnel assisted in aligning the cells in a number of layers and in one direction.

In this setup, the team created microfluidic channels on each side of the cell holding region to replicate blood vessels to imitate the interchange of nutrients and drugs by diffusion in human tissue. The researchers believe that this arrangement may also one day provide the ability to view and gauge the expulsion of metabolic waste from the cells in future experiments.

"Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," said Professor Healy. "It takes about US$5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The use of animal organs to forecast human reactions to new drugs is problematic, the UC Berkeley researchers note, citing the fundamental differences between species as being responsible for high failure rates in using these models. One aspect responsible for this failure is to be found in the difference in the ion channel structure between human and other animals where heart cells conduct electrical currents at different rates and intensities. It is the standardized nature of using actual human heart cells that the team sees as the heart-on-a-chip's distinct advantage over animal models.

The UC Berkeley device is certainly not the first replication of an organ-on-a-chip, but potentially one of the first successful ones to integrate living cells and artificial structures in a single functioning unit. Harvard's spleen-on-a-chip, for example, replicates the operation of the spleen, but does so by using a set of circulatory tubes containing magnetic nanobeads.

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Heart-on-a-chip beats a steady rhythm

WASHINGTON: Researchers, including one of Indian-origin, have created a 'heart-on-a-chip' loaded with human cardiac muscle cells that mimic the real organ to serve as a novel tool to screen medicines. Researchers developed a network of pulsating cardiac muscle cells housed in an inch-long silicone de-vice that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip represents a major step forward in the development of accurate, faster methods of testing for drug toxicity, researchers said. "Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said professor Kevin Healy from the University of California, Berkeley. The authors noted a high failure rate associated with the use of non-human animal models to predict human reactions to new drugs.

"It takes about 5 billion on average to develop a drug, and 60% of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market," said Healy.

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue. Researchers designed their heart-on-a-chip so that its 3D structure would be comparable to the geometry and spacing of connective tissue fibre in a human heart.

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Drug testing on heart-on-a-chip gets a step closer

Cardiac Stem Cells: Making a Difference in Duchenne
Dr Eduardo Marban, Director of the Cedars-Sinai Heart Institute, discusses a possible Cardiac Stem Cell breakthrough for Duchenne muscular dystrophy. Coalition Duchenne founder, Catherine ...

By: CoalitionDuchenne

Excerpt from:
Cardiac Stem Cells: Making a Difference in Duchenne - Video

No Mortality or Toxicity Noted With CryoStor Deployed as Vehicle Solution for Cells and Placebo in Direct Intramyocardial Injections

BioLife Solutions, Inc., a leading developer, manufacturer and marketer of proprietary clinical grade hypothermic storage and cryopreservation freeze media and precision thermal shipping products for cells and tissues (BioLife or the Company), recently announced its CryoStor cell freeze media was utilized in a porcine animal study of umbilical cord blood-derived mononuclear cells (UBC-MNC) to evaluate the safety and feasibility of these cells for cardiac regeneration in pediatric congenital heart disease (CHD).

The safety and feasibility study was performed at the Mayo Clinic in Rochester, Minnesota, with the results recently published in an article titled Safety and Feasibility for Pediatric Cardiac Regeneration Using Epicardial Delivery of Autologous Umbilical Cord Blood-Derived Mononuclear Cells Established in a Porcine Model System, which appeared in the peer reviewed clinical journal Stem Cells Translational Medicine.

Umbilical cord blood-derived mononuclear cells were frozen in protein-free, serum-free CryoStor CS10, containing 10% dimethyl sulfoxide (DMSO). Thawed cells were administered to piglets via intramyocardial injections, with follow up extended to three months. CryoStor CS10 was also used as the placebo control solution without cells, which was injected into randomized piglets.

The authors observed no mortality or toxicity in any study animals and concluded:

Mike Rice, BioLife President & CEO, stated, The data from this study further support the use of our proprietary biopreservation media products in clinical applications. We are quite pleased to have an institution as renowned as the Mayo Clinic evaluate and use our products in their important clinical research.

BioLife management estimates that the Companys CryoStor cryopreservation freeze media andHypoThermosol storage and shipping media have been incorporated into the manufacturing and clinical delivery protocols of more than 175 cell and tissue-based regenerative medicine clinical trials for new products and therapies.

About BioLife Solutions BioLife Solutions develops, manufactures and markets hypothermic storage and cryopreservation solutions and precision thermal shipping products for cells, tissues, and organs. BioLife also performs contract aseptic media formulation, fill, and finish services. The Companys proprietary HypoThermosol and CryoStor platform of solutions are highly valued in the biobanking, drug discovery, and regenerative medicine markets. BioLifes biopreservation media products are serum-free and protein-free, fully defined, and are formulated to reduce preservation-induced cell damage and death. BioLifes enabling technology provides commercial companies and clinical researchers significant improvement in shelf life and post-preservation viability and function of cells, tissues, and organs. For more information, visit http://www.biolifesolutions.com.

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BioLife Solutions CryoStor Cell Freeze Media Used In Mayo Clinic Safety And Feasibility Study Of Umbilical Cord Blood ...