Telomerase helps mend broken hearts

Cardiac muscle regeneration after injury is limited by 'irreversible' cell cycle exit via down-regulation of telomerase reverse transcriptase (TERT). In the August 21 online version of the Proceedings of the National Academy of Sciences, Hidemasa Oh and colleagues from the Baylor College of Medicine, Houston, Texas, show that mice genetically engineered to overexpress TERT produce more and bigger cardiac myocytes, which live longer than those in normal mice.Oh et al. modified mice to express TER

Tudor Toma(t.toma@ic.ac.uk)
Aug 21, 2001

Cardiac muscle regeneration after injury is limited by 'irreversible' cell cycle exit via down-regulation of telomerase reverse transcriptase (TERT). In the August 21 online version of the Proceedings of the National Academy of Sciences, Hidemasa Oh and colleagues from the Baylor College of Medicine, Houston, Texas, show that mice genetically engineered to overexpress TERT produce more and bigger cardiac myocytes, which live longer than those in normal mice.

Oh et al. modified mice to express TERT in cardiac muscle and found that this change was sufficient to rescue telomerase activity and telomere length. Transgenic mice developed a hypercellular ventricle, with increased myocyte density and DNA synthesis and by 12 weeks cardiac cells became hypertrophic. Viral delivery of TERT reproduced the hypertrophy in cultured cardiac myocytes. In addition, the TERT virus and transgene conferred protection from apoptosis, in vitro and in vivo (Proc Natl Acad Sci USA 2001,...

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