HOUSON -- Mice that were genetically engineered to produce a protein found in embryos and stem cells produce more as well as bigger heart cells, which live longer than those in normal mice, according to scientists at Baylor College of Medicine.
The report, in the Aug. 21 online version of the Proceedings of the National Academy of Sciences and in the Aug. 28 printed edition, advances the understanding of how heart muscle cells proliferate and grow and could prove important in treating the 1.5 million Americans who suffer heart attacks each year and the 4.7 million who have congestive heart failure.
“Understanding how this enzyme works gives us new information about normal control of heart muscle growth and could be important in bringing gene-based and cell-based therapies to bear on diseases of the heart,” said Dr. Michael Schneider, senior author of the paper and a professor of medicine, cell biology, and molecular physiology and biophysics at Baylor.
Schneider and his co-workers engineered mice genetically to continue producing the enzyme telomerase reverse transcriptase, or TERT, in heart muscle after birth. TERT enables the ends of the chromosomes, called telomeres, to be copied completely during cell division. Telomeres cap the ends of chromosomes, like plastic tips on shoelaces. Ordinarily, after organisms are born, TERT production stops in most types of cells, and telomeres shorten in the process of aging.
The mice produced in Schneider’s laboratory make TERT at concentrations usually seen only in embryos. In the first month after birth, heart muscle cells in the mice hearts continued to proliferate, dividing and making more cells at a time when there would usually be no new cells. TERT production continued as the mice aged, but eventually the cells stopped dividing and instead grew bigger. This condition, called hypertrophy, usually weakens heart muscle. However, tests show that the hearts in the mice resembled the enlarged organs of healthy, well-trained athletes, without the stiffness seen in heart disease.
Perhaps most importantly from a clinical perspective, Schneider said, mice that continued to express TERT did not lose as many heart muscle cells during a heart attack as normal mice.
“We believe that the effect of adding TERT to an adult heart would be protection from the kind of cell death that occurs during a heart attack as well as production of bigger heart muscle cells,” Schneider said. The enzyme could also be added when cells are grafted onto an injured heart, he said.
Other Baylor collaborators included Drs. Hidemasa Oh, George E. Taffet, Keith A. Youker, Mark L. Entman, Paul A. Overbeek and Lloyd H. Michael.
This work was supported by research grants from the National Heart, Lung, and Blood Institute and by the M. D. Anderson Foundation.
The above post is reprinted from materials provided by Baylor College Of Medicine. Note: Materials may be edited for content and length.
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