Tuesday, February 10, 2015

Telomere extension turns back aging clock in cultured human cells, study finds

News Brief by Fred Lu

Telomeres are 8,000-10,000 nucleotide caps that protect DNA, and shorten with every cell division. This perpetual shrinking is linked to aging and disease – once the telomeres decrease to a certain length, they either stop multiplying and die. Scientists at the Stanford University School of Medicine, led by Helen Blau, Ph.D, have discovered a new way to add 1,000 nucleotides to the ends of human cell chromosomes. This is generally represented as a 10% increase in the length of telomeres and effectively reverses years of aging.

Using modified messenger RNA, the researchers inserted the coding sequence for TERT, the catalytic subunit for the enzyme telomerase, into two different types of human cells. Telomerase is expressed in extremely low levels, except in sperm and eggs cells and is responsible for maintaining telomere length.

After only three applications of the modified RNA, cells in culture divided up to 28 times more than untreated cells. This method marks a significant breakthrough for two reasons – the modified RNA is temporary and it doesn’t cause an immune response against telomerase. The TENT sequence that is added disappears within 48 hours of insertion, which ensures that the targeted cells do not perpetually divide and cause cancer.

The breakthrough allows scientists to examine cells in laboratory for an extended period of time and opens the possibility of treating a multitude of diseases associated with aging or telomere shortening. Blau, along with her colleagues John Ramunas, John Cooke, and Eduard Yakubov, originally became interested in telomeres when they discovered that stem cells from boys affected by Duchenne muscular dystrophy had significantly shortened telomeres. Thanks to this revealation, it may soon be possible to find a cure.

Stanford University Medical Center. "Telomere extension turns back aging clock in cultured human cells, study finds." ScienceDaily. ScienceDaily, 23 January 2015. .
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