Posted on Aug 02, 2017, 8 a.m.
Researchers used a technology called RNA therapeutics to get cells to produce a protein, telomerase, that can extend and lengthen the telomere.
There is no escaping the aging process. A fountain of youth has yet to be discovered. However, scientists are hard at work to make aged cells younger through cellular age-reversal. Houston Methodist researchers have made a discovery that has led to the development of a technology that could rejuvenate the human body's cells. This advancement is certainly welcomed by everyone yet it is particularly important for children who age much more rapidly than others. This condition is referred to as progeria.
The department chair of Houston Methodist Research's cardiovascular sciences division, John P. Cooke, M.D., Ph.D., is at the center of the recent findings. Cooke worked in collaboration with a number of other colleagues to write the research letter “Telomerase mRNA Reverses Senescence in Progeria Cells”. The contributors are as follows: Ivone G. Bruno, Ph.D., Gang Zhou, M.D. and Yanhui Li, M.D., Ph.D. The paper appeared online in the July 31 edition of the Journal of the American College of Cardiology. It will also appear in print in the journal's August 8 edition. The research was supported by grants from the Progeria Research Foundation, the National Institutes of Health and the Cullen Foundation.
About the Findings
Cooke studied cells from children plagued by progeria. His motivation for keying in on progeria patients is that the condition lends valuable insight into the aging process. His aim was to not only improve his understanding of the aging process but also to boost cell function. Cooke's team keyed in on telomeres. These are the timekeepers of cells. They are vitally important for chromosome functionality. Located at the tip of each chromosome, telomeres hold the chromosome together. As one ages, telomeres shrink. Cooke found the telomeres in progeria patients were particularly short. He hypothesized that lengthening these patients' telomeres could boost cell function as well as its ability to respond to stress and divide. Reversing the process of telomere shortening in these children's cells also reversed many of the problems tied to the aging process.
"We all have telomere erosion over time, and many of the things that happen to these children at an accelerated pace occur in all of us," Cooke said. "What we've shown is that when we reverse the process of the telomere shortening in the cells from these children and lengthen them, it can reverse a lot of the problems associated with aging."
The researchers made use of a technology referred to as RNA therapeutics. The cells were stimulated to generate a protein, telomerase, that lengthens telomeres. This was accomplished by providing RNA to cells that encode the protein. Telomerase expressed in cells for a couple days produced a powerful effect on lifespan and cell functionality. The cells proliferated, functioned in a normal manner and divided. The generation of inflammatory proteins was reversed. Cooke noted this approach is superior to other available therapies. Cooke hopes this approach will be used throughout the medical community in the coming years. After all, a large percentage of diseases are a result of the aging process. Aging is an enormous risk factor for vascular diseases and heart disease. Nearly one-third of all United States citizens will endure a stroke or heart attack.
How Cooke's Work is Unique
Cooke's approach is different in that he is not keying on progeria's genetic mutation or the odd protein resulting from mutation. Rather, his team zeroed in on creating a method to boost telomere length in progeria patients. Though his approach won't actually reverse aging at this point, it can produce beneficial effects.
The Next Step
The hope is that Cooke's latest finding will slow down progeria patients' accelerated aging process. Cooke aims to improve existing cell therapies and eventually move them to clinical trials.
Telomerase mRNA Reverses Senescence in Progeria Cells. Journal of the American College of Cardiology. DOI: 10.1016/j.jacc.2017.06.017