Researchers discovered a way to reverse the process of aging in human cell lines.
The scientists found the regulation of two genes involved in the process of producing the amino acid glycine are also responsible for some characteristics of aging, the University of Tsukuba reported. The researchers made the fascinating discovery while investigating a theory that suggests age-associated mitochondrial defects are driven by accumulations of mutations in the mitochondrial DNA.
Abnormal mitochondrial function is associated with aging in most living species, and damage to the mitochondrial DNA creates mutations in the DNA sequence. Accumulations of these mutations have been linked to a reduced lifespan and early symptoms of aging.
The researchers' findings dispute the theory that mitochondrial defects are linked to mutation accumulations, and instead suggest they are caused by another form of genetic regulation. The researchers examined the function of the mitochondria in human fibroblast cell lines derived from both children and the elderly. They compared the mitochondrial respiration and the amount of DNA damage seen in the samples, and found no difference in DNA damage between the two groups. To explain this, the researchers wondered if epigenetic regulation was responsible for the age-associated effects in the mitochondria.
Epigenetic regulations alter the physical structure of DNA, and has the power to switch genes on and off. The idea that they are responsible for aging suggest genetically reprogramming the cells to an embryonic stem cell-like state would eliminate these epigenetic changes.
The researchers reprogrammed human fibroblast cell lines taken from elderly participants to an embryonic stem cell-like state, which were then turned back into turned fibroblasts. The researchers were excited to observe the aging-associated defects were gone, and fibroblasts had had respiration rates closer to what would be seen in a fetal state. The researchers pinpointed the genes CGAT and SHMT2 as the drivers of age-associated mitochondrial defects. By changing the regulation of these genes, mitochondrial function could be restored in the cell lines. The addition of glycine for 10 days to the culture medium of a 97-year-old fibroblast cell line proved to restore respiratory function and reverse age-related respiration defects.
The findings were published in a recent edition of the journal Scientific Reports.
