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• W2249452059 endingPage "23172" @default.
• W2249452059 startingPage "23162" @default.
• W2249452059 abstract "Understanding cell cycle regulation in postmitotic cardiomyocytes may lead to new therapeutic approaches to regenerate damaged cardiac tissue. We have demonstrated previously that microRNAs encoded by the Gtl2-Dio3 noncoding RNA locus function downstream of the MEF2A transcription factor in skeletal muscle regeneration. We have also reported expression of these miRNAs in the heart. Here we investigated the role of two Gtl2-Dio3 miRNAs, miR-410 and miR-495, in cardiac muscle. Overexpression of miR-410 and miR-495 robustly stimulated cardiomyocyte DNA synthesis and proliferation. Interestingly, unlike our findings in skeletal muscle, these miRNAs did not modulate the activity of the WNT signaling pathway. Instead, these miRNAs targeted Cited2, a coactivator required for proper cardiac development. Consistent with miR-410 and miR-495 overexpression, siRNA knockdown of Cited2 in neonatal cardiomyocytes resulted in robust proliferation. This phenotype was associated with reduced expression of Cdkn1c/p57/Kip2, a cell cycle inhibitor, and increased expression of VEGFA, a growth factor with proliferation-promoting effects. Therefore, miR-410 and miR-495 are among a growing number of miRNAs that have the ability to potently stimulate neonatal cardiomyocyte proliferation." @default.
• W2249452059 created "2016-06-24" @default.
• W2249452059 creator A5003583561 @default.
• W2249452059 creator A5056761117 @default.
• W2249452059 date "2015-09-01" @default.
• W2249452059 modified "2023-10-12" @default.
• W2249452059 title "MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2" @default.
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• W2249452059 doi "https://doi.org/10.1074/jbc.m115.672659" @default.
• W2249452059 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4645594" @default.
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• W2249452059 hasPublicationYear "2015" @default.
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