MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading heart

Bao Wei Wang, Gong-Jhe Wu, Wen Ping Cheng, Kou-Gi Shyu

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

MicroRNA-208a (mir-208a) is essential for cardiac hypertrophy and fibrosis. Endoglin, a co-receptor of transforming growth factor-β is also essential for cardiac fibrosis. Endoglin has been shown to be a target of mir-208a in the in vitro mechanical stress model. Volume overload can lead to heart failure and cardiac fibrosis. The role of mir-208a and endoglin in volume overload heart failure is well known. We sought to investigate the mechanism of regulation of mir-208a and endoglin in volume overload-induced heart failure. Aorta-caval (AV) shunt was performed in adult Sprague-Dawley rats to induce volume overload. Heart weight and heart weight/body weight ratio significantly increased in AV shunt animals. AV shunt significantly increased left ventricular end-diastolic dimension as compared to sham group. Mir-208a was significantly induced by AV shunt from 3 to 14 days. Endoglin, myosin heavy chain-β and brain natriuretic peptide were significantly induced by AV shunt from 3 to 14 days. Overexpression of mir-208a in the sham group without AV shunt significantly increased endoglin expression similar to the AV shunt group. Antagomir-208a attenuated the endoglin expression induced by AV shunt. Pretreatment with atorvastatin also attenuated the endoglin expression induced by AV shunt. AV shunt significantly increased myocardial fibrosis as compared to sham group. Overexpression of mir-208a in the sham group significantly increased myocardial fibrosis. Antagomir-208a and atorvastatin significantly attenuated the myocardial fibrosis induced by AV shunt. In conclusion, mir-208a increased endoglin expression to induce myocardial fibrosis in volume overloaded heart failure. Treatment with atorvastatin can attenuate the myocardial fibrosis induced by volume overload through inhibition of endoglin expression.

Original languageEnglish
Article numbere84188
JournalPLoS One
Volume9
Issue number1
DOIs
Publication statusPublished - Jan 2 2014

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Cardiac Volume
fibrosis
MicroRNAs
microRNA
Fibrosis
heart
heart failure
Heart Failure
Myosin Heavy Chains
natriuretic peptides
Brain Natriuretic Peptide
transforming growth factors
vena cava
Transforming Growth Factors
mechanical stress
Endoglin
myosin heavy chains
Weights and Measures
aorta
Rats

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading heart. / Wang, Bao Wei; Wu, Gong-Jhe; Cheng, Wen Ping; Shyu, Kou-Gi.

In: PLoS One, Vol. 9, No. 1, e84188, 02.01.2014.

Research output: Contribution to journalArticle

Wang, Bao Wei ; Wu, Gong-Jhe ; Cheng, Wen Ping ; Shyu, Kou-Gi. / MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading heart. In: PLoS One. 2014 ; Vol. 9, No. 1.
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