Journal
JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
Volume 41, Issue 5, Pages 476-487Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/10799893.2020.1825492
Keywords
Congenital heart disease; human cardiomyocyte progenitor cells; miR-33a-5p; nodal modulator1
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Up-regulation of miR-33a-5p inhibits hCMPCs proliferation, cell cycle G0/S transition, and differentiation into cardiomyocytes but promotes apoptosis by targeting NOMO1. NOMO1 is a target gene of miR-33a-5p, and the up-regulation of miR-33a-5p enhances the expressions of Bax and Caspase-3 while reducing the expressions of Bcl-2, GATA4, cTnT, and MEF2C.
Purpose MicroRNA (miRNA) is known to be involved in the pathological process of congenital heart disease (CHD), and nodal modulator1 (NOMO1) is a critical determinant of heart formation. The present study aims to discover the effect of miR-33a-5p and NOMO1 on CHD. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect expressions of miR-33a-5p mimic or inhibitor and overexpressed NOMO1 plasmid orNOMO1 knockdown. Human cardiomyocyte progenitor cells (hCMPCs) proliferation was measured by cell counting kit-8 (CCK-8) at 24, 48 and 72 h. Flow cytometry was applied to investigate hCMPCs cell cycle progression and apoptosis. Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot. Target genes and potential binding sites of NOMO1 and miR-33a-5p were predicted with Targetscan 7.2, and was confirmed through dual-luciferase reporter assay. Results Up-regulation of miR-33a-5p inhibited hCMPCs proliferation, cell cycle G0/S transition but promoted hCMPCs apoptosis, which was partially mitigated by overexpressed NOMO1. NOMO1 was the target gene of miR-33a-5p. Expressions of Bax and C caspase-3 were enhanced but expressions of Bcl-2, GATA4, cTnT and MEF2C were reduced by up-regulation of miR-33a-5p, which was partially mitigated by overexpressed NOMO1. Conclusion Up-regulation of miR-33a-5p inhibited hCMPCs proliferation, cell cycle G0/S transition and differentiation into cardiomyocytes but promoted apoptosis via targeting NOMO1.
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