Monday, Jul 3, 2006
Aging Process is Out of Our Control
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A study led by Buck Institute faculty member Jan Vijg, PhD, provides the first direct evidence that the molecular machinery of our cells providing function to our tissues and organs spins irreversibly out of control as we age.
Despite our best efforts to increase our chances of longer and healthier old age our cells and tissues ultimately degenerate and eventually die. A study led by Buck Institute faculty member Jan Vijg, PhD, provides the first direct evidence that the molecular machinery of our cells providing function to our tissues and organs spins irreversibly out of control as we age.
The study compared single cells from cardiac tissue in both young and old mice that were genetically identical, bred from the same genetic strain. While at a young age, the different cells displayed very similar activity levels for each gene. At old age, however, they were out of tune, expressing a given gene at sometimes greatly different levels, which is likely to adversely affect the instructions to proteins involved in cardiac tissue function. This is the first time that scientists were able to identify, measure and quantify an increase in gene activity levels in the aged mouse cells, possibly pointing to a random breakdown of gene regulation.
“In younger hearts the cells beat in tune, working together to carry out the functions associated with cardiac tissue,” said Vijg. “As the cells age, they start to diverge, and no longer have the same activity levels. Now that we have a means of identifying and measuring these cell-to-cell variations in gene activity, we can begin to focus on how they cause tissues and organs to become dysfunctional over time,” said Vijg.
One possibility for such an increase in dissimilar gene activity among cells that are supposed to act in a very similar way is that a gradual accumulation of random DNA alterations, also termed “mutations” begin to interfere with transcription, i.e., the process that generates the message from each gene that contains the instructions to make a protein. Such interference can be a result of mutations that cause, for example, a loss of functional gene copies or the inactivation of DNA stretches that serve to control gene activity. To test this possibility, Vijg and his team treated mouse embryo cells with hydrogen peroxide, a free radical-generating agent that damages DNA. In a sense this treatment induces a form of “artificial” aging. The hydrogen peroxide treatment resulted in a significant increase in cell-to-cell variation in gene expression in the embryonic tissue, paralleling the increase found in the cardiac tissue of the older mice.
Vijg, known for his work on DNA damage as a factor in both aging and cancer said, “Genetically, twins are nearly identical when they are young. As they age, their genetic differences become more pronounced. While some differences can likely be attributed to environmental influences, there is little doubt that aging itself is something of a random affair. Indeed, recent work by others provided evidence that the divergence of identical twins also involves alterations in the genome.”
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