Fetal lung tissue used by researchers to measure changes in gene expression associated with cellular aging
Steve Guschmeissner/Science Photo Library
Cellular senescence may be linked to genetic errors that occur over time, which could bring us one step closer to identifying drug targets that slow the process.
Payel Sen of the National Institutes of Health in Maryland previously reported that regulation of gene expression—the process that converts gene-encoded information into function—is broken down in yeast and nematode cells when they stop dividing. discovered that it is still known to produce energy. as senescent cells. Previous studies have shown that in humans, the number of senescent cells increases with age.
To clarify the potential link between gene expression disorders in humans and senescent cells, Sen and her colleagues harvested cultured lung cells from donated human fetuses and treated them very frequently. It was split and aged in 3 months to mimic the aging process.
The team then used a sequencing method called PRO-cap to analyze the length of the newly formed RNA transcripts that make proteins in cells from DNA expression of genes.
Researchers found that these fetal senescent cells produced very short RNA transcripts. These may not be able to make proteins or may make proteins that don’t do what they’re supposed to, says Sen.
Increased variability in gene expression that makes these short transcripts is associated with aging, but we do not know what is happening.
“[The short transcripts] It can rob cells of their life energy and convert it into useless proteins,” she says. “But in reality, we really don’t know.”
In another part of the experiment, the researchers found similar gene expression defects in aged hepatocytes from mice. “The very fact that this is conserved from yeast to mouse to human cells warrants further investigation of the mechanism’s role in aging.
For now, it’s unclear whether senescent cells cause senescence or senescence causes cells to age, she says.
“This study shows that precise regulation of transcription breaks down with age,” says Berenice Benayoun of the University of Southern California. This could provide new targets for drug development to manipulate the aging process, she says.
But, says Jeffrey Craig of Deakin University in Australia, “this enthusiasm also needs to be tempered.” Aging probably has many facets, such as telomere shortening, which occurs when regions of repetitive DNA at the ends of chromosomes shorten over time.
“There may be no one-size-fits-all anti-aging intervention,” he says.
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