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PLoS One. 2014 May 2;9(5):e96290. doi: 10.1371/journal.pone.0096290. eCollection 2014.

Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy.

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Heart Failure Research Center, Academic Medical Center, Amsterdam, The Netherlands; Interuniversitair Cardiologisch Instituut Nederland (ICIN-NHI), Utrecht, The Netherlands.
Heart Failure Research Center, Academic Medical Center, Amsterdam, The Netherlands.
Department of Cell Biology and Histology, Leeuwenhoek Center of Advanced Microscopy (LCAM), Academic Medical Center, Amsterdam, The Netherlands.
Laboratory Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, The Netherlands.


MicroRNAs (miRNAs) regulate many aspects of cellular function and their deregulation has been implicated in heart disease. MiRNA-30c is differentially expressed in the heart during the progression towards heart failure and in vitro studies hint to its importance in cellular physiology. As little is known about the in vivo function of miRNA-30c in the heart, we generated transgenic mice that specifically overexpress miRNA-30c in cardiomyocytes. We show that these mice display no abnormalities until about 6 weeks of age, but subsequently develop a severely dilated cardiomyopathy. Gene expression analysis of the miRNA-30c transgenic hearts before onset of the phenotype indicated disturbed mitochondrial function. This was further evident by the downregulation of mitochondrial oxidative phosphorylation (OXPHOS) complexes III and IV at the protein level. Taken together these data indicate impaired mitochondrial function due to OXPHOS protein depletion as a potential cause for the observed dilated cardiomyopathic phenotype in miRNA-30c transgenic mice. We thus establish an in vivo role for miRNA-30c in cardiac physiology, particularly in mitochondrial function.

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