Heart cells in aged mice contain many more random gene-expression combinations than same cells in young mice

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As we age, our bodies increasingly lose the ability to repair errors that occur in our genetic blueprint, DNA. The errors result in badly formed proteins that perform jobs improperly, resulting in dysfunction that snowballs into conditions such as cancer.

New research, conducted primarily at the Sam and Ann Barshop Institute for Longevity and Aging Studies at the Health Science Center and published June 22 in Nature, reveals a tangible effect of this diminishing lack of correction.

The new work, led by Jan Vijg, Ph.D., who recently joined the Buck Institute for Age Research in Novato, Calif., after several years with the Barshop Institute, indicates that heart-specific genes of older mice no longer produce the instructions to make heart cells (cardiomyocytes) work in the same way as those of younger mice. The activity of these genes, called transcription, varies much more significantly from cell to cell in the aged mice than in their younger counterparts, Dr. Vijg and his team noted.

“These results underscore the stochastic (or random) nature of the aging process, and could provide a mechanism for age-related cellular degeneration and death in tissues of multicellular organisms,” the authors wrote.

Four colleagues from the Barshop Institute, Brad Pollock, Ph.D., M.P.H.; Karl Rodriguez; Ashley Denny; and Gary Chisholm, M.S., are co-authors of the Nature article. Dr. Pollock is professor and director of the Center for Epidemiology and Biostatistics at the Health Science Center.



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