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Epigenetic regulation: turning back the hands of time

by Sasha Crowe Published on 27th May 2015

by Sasha Crowe Published on 27th May 2015

Exciting and pioneering research, led by Professor Jun-Ichi Hayashi from the University of Tsukuba in Japan, into the role epigenetic regulation plays in aging, has been recently published in the journal Nature's Scientific Reports.

While initially performing an experiment looking into the mitochondrial theory of aging, by comparing mitochondrial respiration and DNA damage in old versus young human fibroblast cell lines, they found, contrary to expectation, no difference in the amount of DNA damage within the two groups.
Since the results did not fall in line with the mitochondrial theory of aging, this drove the researchers to find and propose a theory that could explain their findings: epigenetic regulation.

Unlike with the mitochondrial theory of aging, in which abnormal mitochondrial function and defects are the result of an accumulation of mitochondrial DNA mutations, epigenetic regulation deals with genes being turned on or off by changes to the actual structure of the DNA itself whilst keeping the DNA sequence unaffected. Using this theory, it would then technically be possible to genetically restore cells to an embryonic, ‘undamaged’ state by removing the epigenetic changes to the mitochondrial DNA.

By going in the line of thinking that age-related mitochondrial defects are a result of epigenetic regulation,and not through mutations, the researchers were then able to find a way to reverse age-associated mitochondrial defects in both old and young people’s fibroblasts.

They did so by reprogramming human fibroblast cell lines derived from both young and elderly people to an embryonic stem cell-like state, then turning them back into fibroblasts and comparing any difference in respiration rates. By doing so they managed to bring the fibroblast respiratory rates back to a level comparable to those of the fetal fibroblast cell line in both the old and young people's sample, and essentially reverse the age-related defects.

After looking for the epigenetically controlled genes that caused these age-related mitochondrial defects, the researchers found that mitochondrial function could be repaired or damaged by regulating two genes involved with glycine production: CGAT and SHMT2. In further testing, after adding glycine to a 97 year old fibroblast cell line, its respiratory function was restored.

This means that with further testing, as this study suggested, glycine supplements might be an available treatment for older populations in the future.

Read more at ScienceDaily