Mayo Clinic researchers found that two prominent tumor suppressor genes, p16 and p19, play a role in aging. p16 helps accelerate cellular aging, while p19 stops the process.
“Scientists interested in aging have developed mice that lack p16 or p19, but these mice were not suitable for studies on aging because they all die of cancer before they even begin to age,” says the study’s first author, Darren Baker, a laboratory technician at Mayo Clinic and a doctoral candidate. “By crossing these mice with a mouse strain that ages five times faster than normal due to a mutation in the BubR1 gene, we were able to bypass this problem.”
The researchers established that when too much p16 is produced, tissues start to age. Instead of driving aging, the p19 gene was found to counteract the effects of p16. The study also showed that initiation and progression of aging is caused, at least in part, by the accumulation of senescent cells in tissues and organs. These senescent cells have an abnormal gene-expression profile and secrete proteins that damage the surrounding cells, affecting tissue and organ function and aspects of aging.
The findings are published on May 30 in the online issue of Nature Cell Biology.