microRNA-29b Mediates the Antifibrotic Effect of Tanshinone IIA in Postinfarct Cardiac Remodeling

Jan 31, 2015Journal of cardiovascular pharmacology

microRNA-29b helps tanshinone IIA reduce heart scarring after a heart attack

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Abstract

Medium-dose and high-dose Tanshinone IIA significantly inhibited postinfarct cardiac fibrosis in rats.

Tanshinone IIA improved left ventricular function in rats after acute myocardial infarction.
Treatment with Tanshinone IIA downregulated the expression of key proteins involved in fibrosis, including TGF-β1 and collagen types Col1a1 and Col3a1.
Increased levels of miR-29b were observed in cardiac fibroblasts treated with Tanshinone IIA.
Inhibition of miR-29b reduced the antifibrotic effects of Tanshinone IIA, indicating its potential role in this process.
Smad3 signaling is associated with the regulation of miR-29b expression in cardiac fibroblasts.

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BACKGROUND: Tanshinone IIA (TSN) is one of the main components isolated from Danshen, which is widely used for the treatment of cardiovascular diseases. The transforming growth factor beta (TGF-β) signaling pathway and microRNA (miR)-29b play important roles in the progression of cardiac fibrosis and the modulation of cardiac fibroblast (CF) function. Our study investigated the role of miR-29b in the cardioprotective effects of TSN in postinfarct cardiac remodeling.

METHODS AND RESULTS: Echocardiography demonstrated that medium-dose TSN (TSN-M) and high-dose TSN (TSN-H) significantly inhibited postinfarct cardiac fibrosis and improved the impaired left ventricular function in rats subjected to acute myocardial infarction. Moreover, quantitative real-time polymerase chain reaction and Western blot demonstrated that TSN-M and TSN-H downregulated the expression of TGF-β1, Col1a1, Col3a1, and α-SMA but upregulated the expression of miR-29b. CFs treated with TSN showed inhibited TGF-β signaling pathway, downregulated expression of Col1a1, Col3a1, and α-SMA, and upregulated miR-29b expression in vitro. Furthermore, treatment with a miR-29b inhibitor dramatically inhibited these TSN-induced antifibrotic effects, suggesting that miR-29b may be responsible for the antifibrotic effects of TSN. In addition, treatment with Smad3 siRNA significantly inhibited miR-29b expression in CFs, which implies that Smad3 signaling promotes miR-29b expression on CFs.

CONCLUSIONS: TSN exerts antifibrotic effects in postinfarct cardiac fibrosis by upregulating the expression of miR-29b, which is mediated by the TGF-β-Smad3 signaling pathway.

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microRNA-29b Mediates the Antifibrotic Effect of Tanshinone IIA in Postinfarct Cardiac Remodeling

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