Author: ["Alessandra Carè","Daniele Catalucci","Federica Felicetti","Désirée Bonci","Antonio Addario","Paolo Gallo","Marie-Louise Bang","Patrizia Segnalini","Yusu Gu","Nancy D Dalton","Leonardo Elia","Michael V G Latronico","Morten Høydal","Camillo Autore","Matteo A Russo","Gerald W Dorn II","Øyvind Ellingsen","Pilar Ruiz-Lozano","Kirk L Peterson","Carlo M Croce","Cesare Peschle","Gianluigi Condorelli"]
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Abstract
Growing evidence indicates that microRNAs (miRNAs or miRs) are involved in basic cell functions and oncogenesis. Here we report that miR-133 has a critical role in determining cardiomyocyte hypertrophy. We observed decreased expression of both miR-133 and miR-1, which belong to the same transcriptional unit, in mouse and human models of cardiac hypertrophy. In vitro overexpression of miR-133 or miR-1 inhibited cardiac hypertrophy. In contrast, suppression of miR-133 by 'decoy' sequences induced hypertrophy, which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused marked and sustained cardiac hypertrophy. We identified specific targets of miR-133: RhoA, a GDP-GTP exchange protein regulating cardiac hypertrophy; Cdc42, a signal transduction kinase implicated in hypertrophy; and Nelf-A/WHSC2, a nuclear factor involved in cardiogenesis. Our data show that miR-133, and possibly miR-1, are key regulators of cardiac hypertrophy, suggesting their therapeutic application in heart disease.Cite this article
Carè, A., Catalucci, D., Felicetti, F. et al. MicroRNA-133 controls cardiac hypertrophy. Nat Med 13, 613–618 (2007). https://doi.org/10.1038/nm1582 