The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy

Ahmet Ucar, Shashi K. Gupta, Jan Fiedler, Erdem Erikci, Michal Kardasinski, Sandor Batkai, Seema Dangwal, Regalla Kumarswamy, Claudia Bang, Angelika Holzmann, Janet Remke, Massimiliano Caprio, Claudia Jentzsch, Stefan Engelhardt, Sabine Geisendorf, Carolina Glas, Thomas G. Hofmann, Michelle Nessling, Karsten Richter, Mario Schiffer, Lucie Carrier, L. Christian Napp, Johann Bauersachs, Kamal Chowdhury () and Thomas Thum ()
Additional contact information
Ahmet Ucar: Max Planck Institute of Biophysical Chemistry
Shashi K. Gupta: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Jan Fiedler: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Erdem Erikci: Max Planck Institute of Biophysical Chemistry
Michal Kardasinski: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Sandor Batkai: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Seema Dangwal: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Regalla Kumarswamy: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Claudia Bang: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Angelika Holzmann: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Janet Remke: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School
Massimiliano Caprio: Centre for Clinical and Basic Research, IRCCS San Raffaele
Claudia Jentzsch: Institut für Pharmakologie und Toxikologie, Technische Universität München
Stefan Engelhardt: Institut für Pharmakologie und Toxikologie, Technische Universität München
Sabine Geisendorf: Max Planck Institute of Biophysical Chemistry
Carolina Glas: Cellular Senescence Group, Cell and Tumor Biology Program, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance
Thomas G. Hofmann: Cellular Senescence Group, Cell and Tumor Biology Program, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance
Michelle Nessling: Core Facility Electron Microscopy, German Cancer Research Center (DKFZ)
Karsten Richter: Core Facility Electron Microscopy, German Cancer Research Center (DKFZ)
Mario Schiffer: Hannover Medical School
Lucie Carrier: Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf
L. Christian Napp: Hannover Medical School
Johann Bauersachs: Hannover Medical School
Kamal Chowdhury: Max Planck Institute of Biophysical Chemistry
Thomas Thum: Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School

Nature Communications, 2012, vol. 3, issue 1, 1-11

Abstract: Abstract Pathological growth of cardiomyocytes (hypertrophy) is a major determinant for the development of heart failure, one of the leading medical causes of mortality worldwide. Here we show that the microRNA (miRNA)-212/132 family regulates cardiac hypertrophy and autophagy in cardiomyocytes. Hypertrophic stimuli upregulate cardiomyocyte expression of miR-212 and miR-132, which are both necessary and sufficient to drive the hypertrophic growth of cardiomyocytes. MiR-212/132 null mice are protected from pressure-overload-induced heart failure, whereas cardiomyocyte-specific overexpression of the miR-212/132 family leads to pathological cardiac hypertrophy, heart failure and death in mice. Both miR-212 and miR-132 directly target the anti-hypertrophic and pro-autophagic FoxO3 transcription factor and overexpression of these miRNAs leads to hyperactivation of pro-hypertrophic calcineurin/NFAT signalling and an impaired autophagic response upon starvation. Pharmacological inhibition of miR-132 by antagomir injection rescues cardiac hypertrophy and heart failure in mice, offering a possible therapeutic approach for cardiac failure.

Date: 2012
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DOI: 10.1038/ncomms2090

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