Skin is a self-renewing tissue that is required to go through extensive proliferation throughout the lifespan of an organism. Researchers found that telomerase activation plays a significant role in maintenance of skin function and proliferation.
Since telomeres can contribute to the aged appearance of the skin as begin to near the end of their life cycle, at the end of fifty replications of the DNA within the skin cells – the skin can begin to appear aged. With every replication of the DNA, the telomeres becoming shorter and shorter, eventually leading the degradation of the cell leaving the DNA unable to replicate and therefore leading to the aged appearance within the body and the skin.
Researchers at the National Institutes of Health (NIH) say they have identified a new pathway that sets the clock for programmed aging in normal skin and body cells, in a study that was published the Journal of Clinical Investigation. Specificaly the study has focused on the interaction between a toxic protein called progerin and telomeres, which cap the ends of chromosomes like aglets, the plastic tips that bind the ends of shoelaces.
Progerin is a mutated version of a normal cellular protein called lamin A, which is encoded by the normal LMNA gene. Lamin A helps to maintain the normal structure of a cell’s nucleus, the cellular repository of genetic information. Progerin, which has been linked to normal aging, is produced in healthy individuals via “sporadic use of the cryptic splice site”
The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin.
“Telomere shortening during cellular senescence plays a causative role in activating progerin production and leads to extensive change in alternative splicing in multiple other genes,” said lead author Kan Cao, Ph.D., an assistant professor of cell biology and molecular genetics at the University of Maryland, College Park.
The researchers suggest that the combination of telomere fraying and loss with progerin production together induces cell aging. This finding lends insights into how progerin may participate in the normal aging process.
Telomerase is an enzyme that can extend the structure of telomeres so that cells continue to maintain the ability to divide. The study supplied support for the telomere-progerin link, showing that cells that have a perpetual supply of telomerase, known as immortalized cells, produce very little progerin RNA.
So what exactly does the telomerase do to make the cell live forever? This is the really exciting part, and the one that may lead eventually to perpetual youth. As soon as the telomeres split off of a cell when it divides, telomerase acts as a filler to immediately fill in the gap and re-lengthen the telomere. Therefore, the cell doesn’t get short, weaken, and die.
By repairing your skin’s DNA through the activation of telomerase, you can plump up your skin and erase wrinkles, tighten up your sagging jaw line, make your crow’s feet disappear, and banish sun and aging spots.
Source: Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts – Journal of Clinical Investigation, 2011 Jun 13