Parasitic DNA Expands Growth in Aging Tissues

A recent study looks at how parasitic DNA proliferates aging tissues.

As all humans carry "parasitic" strands of DNA that, when not suppressed, copy themselves and spread throughout the genome, these have the potential to affect human health.

According to researchers at Brown University, they found that "retransposable elements" were increasingly able to break free of the genome's control in cultures of human cells. Now researchers found that RTEs are increasingly able to break free and copy themselves in tissues of mice and other aging animals. Other experiments from biologists also showed that activity was really apparent in cancerous tumors that may also be reduced by restricting caloric intake.

"As mice age we are seeing deregulation of these elements and they begin to be expressed and increase in copy number in the genome," said Jill Kreiling, a research assistant professor at Brown, and leader of the study, via a press release. "This may be a very important mechanism in leading to genome instability. A lot of the chronic diseases associated with aging, such as cancer, have been associated with genome instability."

At this time, researchers are uncertain whether the proliferation of RTEs is an exclusively bad thing. However, the question remains that scientists do know that the genome controls RTEs by wrapping them up in a tightly wound configuration known as heterochromatin.

According to Kreiling and co-corresponding author Professor John Sedivy, they found that overall, the genomes from several mouse tissues involved in the study became more heterochromatic with age. However, they also found some signs that the RTEs concentration loosened up when the mice reached a two year mark. This is particularly important because it is associated with chronological aging.

"This brings home the magnitude of the problem," Sedivy said, via the release. "We looked in some pretty major tissues. This appears to be a much more widespread phenomenon. The observation that RTEs become activated with chronological aging of mouse tissues also brings this research in close alignment with very similar discoveries using the fruit fly Drosophila in the labs of Brown Professors Stephen Helfand and Robert Reenan,. The remarkable evolutionary conservation of these fundamental molecular processes indicates that they are likely important aspects of aging. "

Researchers looked at cells from the liver and skeletal muscle of mice at ages 5, 24 and 36 months. When comparing these through gene expression and DNA sequences, they found elevated expression levels in both tissues of many RTEs after 24 months.

However, the RTEs were extremely less successful at proliferating in mice who were fed 40 percent fewer calories. Calorie restriction has been widely shown to create many consequences related to aging in different animal models.

Yet researchers also found that RTEs were more abundant in mouse tissues affected by naturally occurring cancers, including lymphoma and hepatocellular carcinoma.

The study concludes the following, courtesy of the release: "The research does not yet provide evidence that RTEs have a causal role in cancer, Sedivy said. For the time being it's only an association. But he said that researchers have a path forward to study the health consequences of the RTE proliferation that apparently occurs in aging. Certain drugs can inhibit RTE proliferation so researchers should be able to see if doing so extends the amount of time an animal is healthy and free of chronic disease in future mouse experiments."

More information regarding the study can be found via the journal Aging.