Injured skin repairs itself with the help of stem cells, but how this process works isnt well understood. A new study proposes that differentiated skin cells turn back into stem cells to heal the wound.

The process is regulated by a protein called Gata6 made by sebaceous duct cells. In response to injury, these cells migrate out into the skin and de-differentiate into stem cells, which then give rise to replacement skin, according to researchers led by Fiona Watt of Kings College London.

The study was published in Nature Cell Biology. When placed online, the study, Wounding induces dedifferentiation of epidermal Gata6 cells and acquisition of stem cell properties, can be found at j.mp/skincells. Watt was senior author. Giacomo Donati, also of Kings College London, was senior author.

Our data not only demonstrate that the structural and functional complexity of the junctional zone is regulated by Gata6, but also reveal that dedifferentiation is a previously unrecognized property of post-mitotic, terminally differentiated cells that have lost contact with the basement membrane, the study stated.

This resolves the long-standing debate about the contribution of terminally differentiated cells to epidermal wound repair.

One of the most-anticipated results of stem cell research would be generation of replacement tissues for those lost by disease or injury. But the potential for immune rejection limits this potential. While immune-matching can be achieved through patient-derived induced pluripotent stem cells, this process takes time and is costly.

Immune-tolerant allogenic stem cells have been produced in a study reported Monday in Nature Biotechnology. These cells were produced by making them express minimally variant human leukocyte antigen class E molecules. Production of these molecules causes a self response that inhibits attack by NK natural killer cells.

When published, the study, HLA-E-expressing pluripotent stem cells escape allogeneic responses and lysis by NK cells, can be found online at j.mp/allogenic. David W Russell was senior author and Germn Gornalusse was first author. Both are of University of Washington, Seattle.

A study conducted in a mouse model of spinal muscular atrophy suggests that symptoms might be reduced by increasing the activity of synapses between sensory and motor neurons. It suggests there may be more than one path to improving or preserving muscle function in SMA patients.

SMA is caused by the deterioration and eventual death of spinal motor neurons. The only treatment shown to affect the underlying course of the disease, Spinraza, was researched by Ionis Pharmaceuticals in Carlsbad and brought to market in a partnership with Biogen.

The study was published Monday in Nature Neuroscience. George Z Mentis was the senior author and Emily V Fletcher was first author. Both are of Columbia University in New York. When placed online, the study, Reduced sensory synaptic excitation impairs motor neuron function via Kv2.1 in spinal muscular atrophy, can be found at j.mp/smanew.

Researchers treated the mice with kainate, which restored near-normal synaptic functioning and improved motor functioning. While the chemical induces seizures, the mice were given doses lower than the seizure threshold.

Because of kainates seizure-inducing potential, the researchers are looking for safer chemicals to stimulate the synaptic connections.

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Skin regeneration, universal donor stem cells and new SMA treatment approach - The San Diego Union-Tribune