The main function of adult stem cells is to enable the replacement of old or damaged cells of most types, from neurons to skin to the liver. One of the main reasons that organisms as a whole suffer from aging is that their adult stem cells do too, almost like any other cell type.
An important differences between stem cells and other types of cells is that there is a limit to how often an ordinary cell can divide (to create new cells of the same type). This limit is controlled by telomeres – structures on the ends of chromosomes that are gradually shortened every time a cell divides, in part because DNA copying mechanisms cannot accurately copy the ends of DNA strands. In stem cells, however, a mechanism is active that can rebuild shortened telomeres. (This also happens in cancer cells, unfortunately.)
However, in spite of telomere repair in stem cells, they still experience aging, so there must be more to aging than telomeres. One factor is the accumulation of DNA damage due to the inherent imperfections in DNA repair mechanisms.
The research in question here compared young adult stem cells with cells of the same type that had been allowed to divide repeatedly in cultures, in order to determine what changed. One important difference found was the accumulation of DNA segments called Alu element retrotransposons. This type of noncoding DNA is common in primate genomes. However, the accumulation that occurs in aging stem cells appears to be toxic to the cells and eventually forces them into a senescent state.
The good news is that when copying of these Alu elements is suppressed, stem cells are able to regain their self-renewing properties. Naturally, this is being investigated further for possible applications in slowing the overall aging process.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
“We demonstrated that we were able to reverse the process of aging for human adult stem cells by intervening with the activity of non-protein coding RNAs originated from genomic regions once dismissed as non-functional ‘genomic junk’,” said Victoria Lunyak, associate professor at the Buck Institute for Research on Aging.