Ezh2 is not required for cardiac regeneration in neonatal mice

PloS One
Abdalla AhmedPaul Delgado-Olguin

Abstract

The neonatal mouse heart has the remarkable capacity to regenerate lost myocardium within the first week of life. Neonatal cardiomyocytes re-express fetal genes that control cell proliferation after injury to promote regeneration. The loss of regenerative capacity of the heart one week after birth coincides with repression of a fetal transcriptional program coordinated by epigenetic regulators. The histone methyltransferase enhancer of zeste homolog 2 (Ezh2) is a repressor of fetal cardiac transcriptional programs and suppresses cardiomyocyte cell proliferation, suggesting a potential function in heart regeneration. However, it was recently demonstrated that Ezh2 is dispensable for heart regeneration in the neonatal heart. Here, we provide evidence supporting this finding and demonstrate that Ezh2 deficiency does not affect regeneration of the neonatal heart. We inactivated Ezh2 in differentiating embryonic cardiomyocytes, which led to depletion of histone H3 trimethylated at lysine 27 (H3K27me3). Ezh2 deficiency in cardiomyocytes did not affect clearance of the fibrotic scar in myocardial infarction (MI) and apical resection models of cardiac injury at post-natal day 1 (P1). Similarly, cardiomyocyte-specific loss of Ezh2 did n...Continue Reading

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Citations

Dec 21, 2018·Circulation·Nicholas T Lam, Hesham A Sadek
Apr 26, 2020·Current Cardiology Reports·Alisson C CardosoHesham A Sadek
Aug 22, 2020·American Journal of Physiology. Heart and Circulatory Physiology·Marta W SzulikSarah Franklin
Feb 9, 2021·Frontiers in Physiology·Francisco SantosBruno Bernardes de Jesus
May 25, 2021·Journal of Cardiovascular Pharmacology·Jia-Li YuanQun-Shan Wang

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