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Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy. / Wijnen, Wino J.; van der Made, Ingeborg; van den Oever, Stephanie et al.

In: PLoS ONE, Vol. 9, No. 5, 2014, p. e96290.

Research output: Contribution to journal › Article › Academic › peer-review

Harvard

Wijnen, WJ, van der Made, I, van den Oever, S, Hiller, M, de Boer, BA, Picavet, DI, Chatzispyrou, IA, Houtkooper, RH, Tijsen, AJ, Hagoort, J, van Veen, H, Everts, V, Ruijter, JM, Pinto, YM & Creemers, EE 2014, 'Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy', PLoS ONE, vol. 9, no. 5, pp. e96290. https://doi.org/10.1371/journal.pone.0096290

APA

Wijnen, W. J., van der Made, I., van den Oever, S., Hiller, M., de Boer, B. A., Picavet, D. I., Chatzispyrou, I. A., Houtkooper, R. H., Tijsen, A. J., Hagoort, J., van Veen, H., Everts, V., Ruijter, J. M., Pinto, Y. M., & Creemers, E. E. (2014). Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy. PLoS ONE, 9(5), e96290. https://doi.org/10.1371/journal.pone.0096290

Vancouver

Wijnen WJ, van der Made I, van den Oever S, Hiller M, de Boer BA, Picavet DI et al. Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy. PLoS ONE. 2014;9(5):e96290. doi: 10.1371/journal.pone.0096290

Author

Wijnen, Wino J. ; van der Made, Ingeborg ; van den Oever, Stephanie et al. / Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy. In: PLoS ONE. 2014 ; Vol. 9, No. 5. pp. e96290.

BibTeX

@article{845b1caf8cba4f45a3a9688cf744c545,
title = "Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy",
abstract = "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",
author = "Wijnen, {Wino J.} and {van der Made}, Ingeborg and {van den Oever}, Stephanie and Monika Hiller and {de Boer}, {Bouke A.} and Picavet, {Daisy I.} and Chatzispyrou, {Iliana A.} and Houtkooper, {Riekelt H.} and Tijsen, {Anke J.} and Jaco Hagoort and {van Veen}, Henk and Vincent Everts and Ruijter, {Jan M.} and Pinto, {Yigal M.} and Creemers, {Esther E.}",
year = "2014",
doi = "10.1371/journal.pone.0096290",
language = "English",
volume = "9",
pages = "e96290",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy

AU - Wijnen, Wino J.

AU - van der Made, Ingeborg

AU - van den Oever, Stephanie

AU - Hiller, Monika

AU - de Boer, Bouke A.

AU - Picavet, Daisy I.

AU - Chatzispyrou, Iliana A.

AU - Houtkooper, Riekelt H.

AU - Tijsen, Anke J.

AU - Hagoort, Jaco

AU - van Veen, Henk

AU - Everts, Vincent

AU - Ruijter, Jan M.

AU - Pinto, Yigal M.

AU - Creemers, Esther E.

PY - 2014

Y1 - 2014

N2 - 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

AB - 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

U2 - 10.1371/journal.pone.0096290

DO - 10.1371/journal.pone.0096290

M3 - Article

C2 - 24789369

VL - 9

SP - e96290

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 5

ER -

ID: 2399107