These results reveal a previously unrecognized critical role for cyclin A2 in mediating cardiomyocyte mitosis, a role that may significantly impact upon clinical treatment of damaged myocardium. Magnetic resonance analysis confirmed cardiac enlargement. Several stages of mitosis were observed within cardiomyocytes and correlated with the nuclear localization of cyclin A2. Cardiomyocyte hyperplasia during adulthood was coupled with an increase in cardiomyoctye mitosis, noted in transgenic hearts at all time points examined, particularly during postnatal development. We now report that cyclin A2, normally silenced in the postnatal heart, induces cardiac enlargement because of cardiomyocyte hyperplasia when constitutively expressed from embryonic day 8 into adulthood. Previous reports describing manipulation of cell cycle proteins have not shown induction of cardiomyocyte mitosis after birth. Therefore, the concept of stimulating myocyte mitotic divisions has dramatic implications for cardiomyocyte regeneration and hence, cardiovascular disease. peak in sites losing binding in mitosis (LOST) or retaining binding (BOOK). Cell cycle withdrawal limits proliferation of adult mammalian cardiomyocytes. By maintaining nucleosome positioning during mitosis, ESRRB might ensure the.
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