Soluble transforming growth factor-β1 receptor II might inhibit transforming growth factor-β-induced myofibroblast differentiation and improve ischemic cardiac function after myocardial infarction in rats

Jul 9, 2010Coronary artery disease

A soluble receptor may block scar-forming cell changes and improve heart function after heart attack in rats

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Abstract

Administration of soluble TGF-beta1 receptor II (sTbetaRII) improved cardiac function and reduced fibrosis in myocardial infarction rats.

sTbetaRII significantly decreased cell proliferation, myofibroblast differentiation, and expression of P-Smad2 in cardiac fibroblasts compared to TGF-beta1 treatment.
Two weeks post-administration, myofibroblast differentiation was reduced in myocardial infarction rats treated with sTbetaRII compared to those that did not receive it.
Four weeks after sTbetaRII treatment, rats showed significant improvements in cardiac function along with reductions in weight parameters, infarct size, and collagen fiber content.

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OBJECTIVE: Cardiac fibroblasts (CFs) regulate myocardial fibrosis and remodeling through proliferation and differentiation. Transforming growth factor-beta1 (TGF-beta1) plays a critical role in the development of myocardial fibrosis after myocardial infarction (MI). The aim of this study was to investigate the effects of inhibiting TGF-beta1 action on myofibroblast differentiation and cardiac function after MI.

METHODS: CFs were cultured and treated, respectively with PBS, TGF-beta1, soluble TGF-beta1 receptor II (sTbetaRII), and TGF-beta1 plus sTbetaRII. Proliferation CFs were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Myofibroblast differentiation was examined by alpha-smooth muscle actin immunostaining. Expression of P-Smad2 and Smad2/3 was determined by immunostaining and western blot analysis. Four days after ligation of left anterior descending coronary artery, sTbetaRII was injected into injured heart. Two weeks after sTbetaRII administration, myofibroblast differentiation was measured with alpha-smooth muscle actin immunostaining. Four weeks after sTbetaRII administration, cardiac function was evaluated by hemodynamic measurements. Weight parameters, infarct size, and collagen fiber were detected with an earlier experimental method.

RESULTS: Compared with TGF-beta1, TGF-beta1 plus sTbetaRII significantly decreased cell proliferation, myofibroblast differentiation, and expression of P-Smad2 in CFs (P<0.05). Two weeks after sTbetaRII administration, myofibroblast differentiation in MI rats treated with sTbetaRII was reduced compared with MI group (P<0.05). Four weeks after sTbetaRII administration, MI rats that received sTbetaRII showed significantly higher cardiac function and lower in weight parameters, infarct size, and collagen fiber than that of MI group (P<0.05).

CONCLUSION: sTbetaRII could inhibit TGF-beta1-induced myofibroblast differentiation, alleviate myocardial fibrosis and remodeling, and improve ischemic cardiac function after MI.

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Soluble transforming growth factor-β1 receptor II might inhibit transforming growth factor-β-induced myofibroblast differentiation and improve ischemic cardiac function after myocardial infarction in rats

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