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MicroRNA-133 controls cardiac myocyte hypertrophy (Articolo in rivista)

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MicroRNA-133 controls cardiac myocyte hypertrophy (Articolo in rivista) (literal)

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Carè A; Catalucci D; Felicetti F; Bonci D; Addario A; Gallo P; Bang ML; Segnalini P; Gu Y; Dalton ND; Elia L; Latronico MV; Høydal M; Autore C; Russo MA; Dorn GW 2nd; Ellingsen O; Ruiz-Lozano P; Peterson KL; Croce CM; Peschle C; Condorelli G (2007)
MicroRNA-133 controls cardiac myocyte hypertrophy
in Nature medicine (Online); NATURE PUBLISHING GROUP,, LONDON (Regno Unito)
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Carè A; Catalucci D; Felicetti F; Bonci D; Addario A; Gallo P; Bang ML; Segnalini P; Gu Y; Dalton ND; Elia L; Latronico MV; Høydal M; Autore C; Russo MA; Dorn GW 2nd; Ellingsen O; Ruiz-Lozano P; Peterson KL; Croce CM; Peschle C; Condorelli G (literal)

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Department of Medicine, Division of Cardiology, University of California San Diego, La Jolla, California 92093, USA. Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore Sanita` , 00161 Rome, Italy. Istituto di Ricovero e Cura a Carattere Scientifico Multimedica, 20099 Milan, Italy. San Raffaele Biomedical Science Park, 00128 Rome, Italy. The Norwegian University of Science and Technology (NTNU), 7491 Trondheim, Norway. 6II Faculty of Medicine, University 'La Sapienza', 00161 Rome, Italy. Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Pisana, 00163 Rome, Italy. Division of Cardiology, University of Cincinnati, Cincinnati, Ohio 45267, USA. The Burnham Institute for Medical Research, La Jolla, California 92037, USA. Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210, USA. (literal)

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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. (literal)

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