Finally, mitosis in adult cardiomyocytes is associated with transient dedifferentiation of the contractile apparatus. Furthermore, inhibition of p38 in adult cardiomyocytes promotes cytokinesis. In contrast, cardiac-specific p38α knockout mice show a 92.3% increase in neonatal cardiomyocyte mitoses. Activation of p38 in vivo by MKK3bE reduces BrdU incorporation in fetal cardiomyocytes by 17.6%. p38 activity is inversely correlated with cardiac growth during development, and its overexpression blocks fetal cardiomyocyte proliferation. p38 regulates expression of genes required for mitosis in cardiomyocytes, including cyclin A and cyclin B. One important mechanism used by mammalian cardiomyocytes to control cell cycle is p38 MAP kinase activity. Here, we show that adult mammalian cardiomyocytes can divide. Consequently, acutely injured mammalian hearts do not regenerate, they scar. Adult mammalian cardiomyocytes are considered terminally differentiated and incapable of proliferation.
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