A gene that has the potential to suppress tumor growth also plays a major role in aging, according to three separate studies. The gene p16INK4a caused cell to grow old and work poorly as compared to younger cells.// These older cells seemed to know their age even when transplanted into young mice. Other cells in the young mice were not as sluggish as these older cells.
Teams from the medical schools at the University of North Carolina at Chapel Hill, University of Michigan and Harvard University observed similar results in pancreatic islet cells and brain and blood stem cells.
The results show disparate cell types share a common aging mechanism and suggest that aging-related diseases such as diabetes result from a failure of cell growth, said Dr. Norman E. Sharpless, co-author on the three studies and an assistant professor of medicine and genetics at the UNC School of Medicine. 'The studies indicate that certain stem cells lose their ability to divide and replace themselves with age as the expression of p16INK4a increases,' said Sharpless, a member of the UNC Lineberger Comprehensive Cancer Center.
The trio of reports are published online Sept. 6 in the journal Nature. The three research teams are from the medical schools at UNC, the University of Michigan and Harvard University.
The UNC study focused on p16INK4a effects on the function of pancreatic islet cells. Islet cells are responsible for insulin production and secretion. Because p16INK4a stops cancer cells from dividing and demonstrates increased expression with age, the scientists suspected the gene played a similar role in aging. The researchers developed strains of mice that were either deficient in p16INK4a (the gene was deleted, or 'knocked out') or genetically altered to have an excess of the protein to a degree seen in aging.
According to Sharpless, islet proliferation persisted in p16INK4a -deficient animals as they aged, 'almost as if they were yPage: 1 2 3 Related medicine news :1
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