MicroRNA-208a increases myocardial endoglin expression and myocardial fibrosis in acute myocardial infarction

Kou Gi Shyu, Bao Wei Wang, Wen Pin Cheng, Huey Ming Lo

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background: MicroRNAs (miRs) play a role in cardiac remodelling, and acute myocardial infarction (AMI) can regulate miR expression. MiR-208a is essential for the expression of the genes involved in cardiac hypertrophy and fibrosis. MiR-208a activates endoglin expression and may result in cardiac fibrosis. The role of miR-208a and endoglin in AMI is not known. We sought to investigate the regulation of miR-208a and endoglin in AMI. Methods: Ligation of the proximal left anterior descending artery was performed in adult Sprague-Dawley rats to induce AMI. Echocardiography was used to measure heart size and left ventricular function. The TaqMan miR real-time quantitative assay was used to quantitate miR-208a. Myocardial fibrosis was detected by Masson trichrome staining. Results: AMI and overexpression of miR-208a in the sham group without infarction significantly increased myocardial miR-208a, endoglin, and β-myosin heavy chain (β-MHC) expression. Overexpression of antagomir-208a significantly inhibited the increase of myocardial endoglin and β-MHC protein expression induced by infarction. Overexpression of mutant miR-208a in the sham group did not induce myocardial endoglin and β-MHC expression. Pretreatment with atorvastatin and the angiotensin-receptor antagonist valsartan significantly attenuated the increase of endoglin and β-MHC induced by infarction. AMI and overexpression of miR-208a in the sham group significantly increased the area of myocardial fibrosis compared with the sham group. Overexpression of antagomir-208a and pretreatment with atorvastatin and valsartan in the AMI group significantly decreased the area of myocardial fibrosis induced by infarction. Conclusions: MiR-208a increases endoglin expression to induce myocardial fibrosis in rats with AMI. Treatment with atorvastatin and valsartan can decrease myocardial fibrosis induced by AMI through attenuating miR-208a and endoglin expression.

Original languageEnglish
Pages (from-to)679-690
Number of pages12
JournalCanadian Journal of Cardiology
Volume31
Issue number5
DOIs
Publication statusPublished - May 1 2015

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MicroRNAs
Fibrosis
Myocardial Infarction
Valsartan
Infarction
Endoglin
Myosin Heavy Chains
Angiotensin Receptor Antagonists
Essential Genes
Cardiomegaly
Left Ventricular Function
Ligation
Sprague Dawley Rats
Echocardiography
Arteries
Staining and Labeling

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

MicroRNA-208a increases myocardial endoglin expression and myocardial fibrosis in acute myocardial infarction. / Shyu, Kou Gi; Wang, Bao Wei; Cheng, Wen Pin; Lo, Huey Ming.

In: Canadian Journal of Cardiology, Vol. 31, No. 5, 01.05.2015, p. 679-690.

Research output: Contribution to journalArticle

Shyu, Kou Gi ; Wang, Bao Wei ; Cheng, Wen Pin ; Lo, Huey Ming. / MicroRNA-208a increases myocardial endoglin expression and myocardial fibrosis in acute myocardial infarction. In: Canadian Journal of Cardiology. 2015 ; Vol. 31, No. 5. pp. 679-690.
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AB - Background: MicroRNAs (miRs) play a role in cardiac remodelling, and acute myocardial infarction (AMI) can regulate miR expression. MiR-208a is essential for the expression of the genes involved in cardiac hypertrophy and fibrosis. MiR-208a activates endoglin expression and may result in cardiac fibrosis. The role of miR-208a and endoglin in AMI is not known. We sought to investigate the regulation of miR-208a and endoglin in AMI. Methods: Ligation of the proximal left anterior descending artery was performed in adult Sprague-Dawley rats to induce AMI. Echocardiography was used to measure heart size and left ventricular function. The TaqMan miR real-time quantitative assay was used to quantitate miR-208a. Myocardial fibrosis was detected by Masson trichrome staining. Results: AMI and overexpression of miR-208a in the sham group without infarction significantly increased myocardial miR-208a, endoglin, and β-myosin heavy chain (β-MHC) expression. Overexpression of antagomir-208a significantly inhibited the increase of myocardial endoglin and β-MHC protein expression induced by infarction. Overexpression of mutant miR-208a in the sham group did not induce myocardial endoglin and β-MHC expression. Pretreatment with atorvastatin and the angiotensin-receptor antagonist valsartan significantly attenuated the increase of endoglin and β-MHC induced by infarction. AMI and overexpression of miR-208a in the sham group significantly increased the area of myocardial fibrosis compared with the sham group. Overexpression of antagomir-208a and pretreatment with atorvastatin and valsartan in the AMI group significantly decreased the area of myocardial fibrosis induced by infarction. Conclusions: MiR-208a increases endoglin expression to induce myocardial fibrosis in rats with AMI. Treatment with atorvastatin and valsartan can decrease myocardial fibrosis induced by AMI through attenuating miR-208a and endoglin expression.

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