Protein determines aging processes in different cells
A specific protein appears to control the aging of various tissue cells, three research groups have discovered. The protein called p16INK4a was already known to stop cell division and tumor growth.
The working group of Sean Morrison from the University of Michigan at Ann Arbor has now investigated the influence of p16INK4a on neurogenesis in the forebrain . Norman Sharpless from the University of North Carolina at Chapel Hill and his colleagues were interested in the role of the tumor suppressor in the insulin-producing islet cells of the pancreas . And the researchers led by David Scadden from Massachusetts General Hospital in Boston concentrated on the blood-forming stem cells of the bone marrow .
All three working groups came to the same conclusion: in mice with the p16INK4a gene switched off, typical aging processes were reduced. Both the neuronal progenitor cells in the brain and the progenitors of the islet cells in the pancreas and the hematopoietic stem cells in the bone marrow retained their ability to divide. Conversely, in genetically engineered mice that produced an excess of p16INK4a, the stem cells rapidly slowed down their proliferation rate.
The researchers suspect that the protein could also be involved in diabetes: Too much of it may disrupt insulin production in the islet cells - which in turn could be treated by blocking the protein with drugs.
But blocking p16INK4a will not be a fountain of youth, the researchers warn: Mice lacking the protein did not live any longer than their normal peers. Without the antitumor effect of p16INK4a they were more likely to die of cancer.