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Telomere extension turns back aging clock (2015-02-04)

A new procedure can quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are linked to aging and disease, according to scientists at the Stanford University School of Medicine.
New research in The FASEB Journal suggests thatdelivering modified mRNA encoding the protein telomerase reverse transcriptase (TERT) to cells extends their telomeres a finite but significant amount.

One of the key aspects of aging is the shortening of telomeres over time. Telomeres, which serve as protective "end caps" for chromosomes, help keep DNA healthy and functioning as it replicates. Unfortunately, these protective end caps become shorter with each DNA replication, and eventually are no longer able to protect DNA from sustaining damage and mutations. In other words, we get older.

Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells. The research may point to new ways to treat diseases caused by shortened telomeres.

In young humans, telomeres are about 8,000-10,000 nucleotides long. They shorten with each cell division, however, and when they reach a critical length the cell stops dividing or dies. This internal "clock" makes it difficult to keep most cells growing in a laboratory for more than a few cell doublings.
"Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life," said Helen Blau, PhD, professor of microbiology and immunology at Stanford and director of the university's Baxter Laboratory for Stem Cell Biology. "This greatly increases the number of cells available for studies such as drug testing or disease modeling."

The newly developed technique has an important advantage over other potential methods: It's temporary. The modified RNA is designed to reduce the cell's immune response to the treatment and allow the TERT-encoding message to stick around a bit longer than an unmodified message would. But it dissipates and is gone within about 48 hours. After that time, the newly lengthened telomeres begin to progressively shorten again with each cell division.

The transient effect is somewhat like tapping the gas pedal in one of a fleet of cars coasting slowly to a stop. The car with the extra surge of energy will go farther than its peers, but it will still come to an eventual halt when its forward momentum is spent. On a biological level, this means the treated cells don't go on to divide indefinitely, which would make them too dangerous to use as a potential therapy in humans because of the risk of cancer.

"This new approach paves the way toward preventing or treating diseases of aging," said Blau. "There are also highly debilitating genetic diseases associated with telomere shortening that could benefit from such a potential treatment."

For more information
Stanford Medicine

The FASEB Journal
Transient delivery of modified mRNA encoding TERT rapidly extends telomeres in human cells

MDN