Nanog May Improve Function of Old Stem Cells

In this research, the scientists involved investigate a potential role for the gene nanog in the aging of stem cells, a prospect that has been studied for a few years now. Nanog is involved in pluripotency, the ability of embryonic stem cells to generate any cell type, but, as is the case for most cellular biology, not in a straightforward way. In recent years, with the development of induced pluripotent stem cells, a great deal of attention has been directed towards the molecular biology of genes such as nanog.

To battle aging, the human body holds a reservoir of nonspecialized cells that can regenerate organs. These cells are called adult stem cells, and they are located in every tissue of the body and respond rapidly when there is a need. But as people age, fewer adult stem cells perform their job well, a scenario which leads to age-related disorders. Reversing the effects of aging on adult stem cells, essentially rebooting them, can help overcome this problem.

In the new study, researchers introduced Nanog into aged smooth muscle stem cells and found that Nanog opens two key cellular pathways: Rho-associated protein kinase (ROCK) and Transforming growth factor beta (TGF-β). In turn, this jumpstarts dormant proteins (actin) into building cytoskeletons that adult stem cells need to form muscle cells that contract. Force generated by these cells ultimately helps restore the regenerative properties that adult stem cells lose due to aging.

Additionally, the researchers showed that Nanog activated the central regulator of muscle formation, serum response factor (SRF), suggesting that the same results may be applicable for skeletal, cardiac and other muscle types. The researchers are now focusing on identifying drugs that can replace or mimic the effects of NANOG. This will allow them to study whether aspects of aging inside the body can also be reversed. This could have implications in an array of illnesses, everything from atherosclerosis and osteoporosis to Alzheimer's disease.

Link: http://www.buffalo.edu/news/releases/2016/07/023.html

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