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

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The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. / Ucar, Ahmet; Gupta, Shashi K; Fiedler, Jan; Erikci, Erdem; Kardasinski, Michal; Batkai, Sandor; Dangwal, Seema; Kumarswamy, Regalla; Bang, Claudia; Holzmann, Angelika; Remke, Janet; Caprio, Massimiliano; Jentzsch, Claudia; Engelhardt, Stefan; Geisendorf, Sabine; Glas, Carolina; Hofmann, Thomas G; Nessling, Michelle; Richter, Karsten; Schiffer, Mario; Carrier, Lucie; Napp, L Christian; Bauersachs, Johann; Chowdhury, Kamal; Thum, Thomas.

In: NAT COMMUN, Vol. 3, 2012, p. 1078.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ucar, A, Gupta, SK, Fiedler, J, Erikci, E, Kardasinski, M, Batkai, S, Dangwal, S, Kumarswamy, R, Bang, C, Holzmann, A, Remke, J, Caprio, M, Jentzsch, C, Engelhardt, S, Geisendorf, S, Glas, C, Hofmann, TG, Nessling, M, Richter, K, Schiffer, M, Carrier, L, Napp, LC, Bauersachs, J, Chowdhury, K & Thum, T 2012, 'The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy.', NAT COMMUN, vol. 3, pp. 1078. https://doi.org/10.1038/ncomms2090

APA

Ucar, A., Gupta, S. K., Fiedler, J., Erikci, E., Kardasinski, M., Batkai, S., Dangwal, S., Kumarswamy, R., Bang, C., Holzmann, A., Remke, J., Caprio, M., Jentzsch, C., Engelhardt, S., Geisendorf, S., Glas, C., Hofmann, T. G., Nessling, M., Richter, K., ... Thum, T. (2012). The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. NAT COMMUN, 3, 1078. https://doi.org/10.1038/ncomms2090

Vancouver

Ucar A, Gupta SK, Fiedler J, Erikci E, Kardasinski M, Batkai S et al. The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. NAT COMMUN. 2012;3:1078. https://doi.org/10.1038/ncomms2090

Bibtex

@article{d49ef69b655f47c19cf8fd1faf53b220,
title = "The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy.",
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.",
keywords = "Animals, Male, Cells, Cultured, Mice, Rats, Reverse Transcriptase Polymerase Chain Reaction, Mice, Transgenic, MicroRNAs/*genetics, Myocytes, Cardiac/*metabolism, Autophagy/*genetics, Calcineurin/genetics, Cardiomegaly/*genetics, Oligonucleotides/*genetics, Animals, Male, Cells, Cultured, Mice, Rats, Reverse Transcriptase Polymerase Chain Reaction, Mice, Transgenic, MicroRNAs/*genetics, Myocytes, Cardiac/*metabolism, Autophagy/*genetics, Calcineurin/genetics, Cardiomegaly/*genetics, Oligonucleotides/*genetics",
author = "Ahmet Ucar and Gupta, {Shashi K} and Jan Fiedler and Erdem Erikci and Michal Kardasinski and Sandor Batkai and Seema Dangwal and Regalla Kumarswamy and Claudia Bang and Angelika Holzmann and Janet Remke and Massimiliano Caprio and Claudia Jentzsch and Stefan Engelhardt and Sabine Geisendorf and Carolina Glas and Hofmann, {Thomas G} and Michelle Nessling and Karsten Richter and Mario Schiffer and Lucie Carrier and Napp, {L Christian} and Johann Bauersachs and Kamal Chowdhury and Thomas Thum",
year = "2012",
doi = "10.1038/ncomms2090",
language = "English",
volume = "3",
pages = "1078",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy.

AU - Ucar, Ahmet

AU - Gupta, Shashi K

AU - Fiedler, Jan

AU - Erikci, Erdem

AU - Kardasinski, Michal

AU - Batkai, Sandor

AU - Dangwal, Seema

AU - Kumarswamy, Regalla

AU - Bang, Claudia

AU - Holzmann, Angelika

AU - Remke, Janet

AU - Caprio, Massimiliano

AU - Jentzsch, Claudia

AU - Engelhardt, Stefan

AU - Geisendorf, Sabine

AU - Glas, Carolina

AU - Hofmann, Thomas G

AU - Nessling, Michelle

AU - Richter, Karsten

AU - Schiffer, Mario

AU - Carrier, Lucie

AU - Napp, L Christian

AU - Bauersachs, Johann

AU - Chowdhury, Kamal

AU - Thum, Thomas

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

KW - Animals

KW - Male

KW - Cells, Cultured

KW - Mice

KW - Rats

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Mice, Transgenic

KW - MicroRNAs/genetics

KW - Myocytes, Cardiac/metabolism

KW - Autophagy/genetics

KW - Calcineurin/genetics

KW - Cardiomegaly/genetics

KW - Oligonucleotides/genetics

KW - Animals

KW - Male

KW - Cells, Cultured

KW - Mice

KW - Rats

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Mice, Transgenic

KW - MicroRNAs/genetics

KW - Myocytes, Cardiac/metabolism

KW - Autophagy/genetics

KW - Calcineurin/genetics

KW - Cardiomegaly/genetics

KW - Oligonucleotides/genetics

U2 - 10.1038/ncomms2090

DO - 10.1038/ncomms2090

M3 - SCORING: Journal article

VL - 3

SP - 1078

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -