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

Autor: Zenglu Xu, Yuejie Chen, Xiaodong Zhang, Ruiqing Lian
Rok vydání: 2010
Předmět:
Cardiac function curve
medicine.medical_specialty
Time Factors
Microinjections
Blotting
Western
Myocardial Infarction
Smad2 Protein
Protein Serine-Threonine Kinases
Ventricular Function
Left
Rats
Sprague-Dawley
Transforming Growth Factor beta1
Fibrosis
Internal medicine
Ventricular Pressure
medicine
Animals
Smad3 Protein
Myocardial infarction
Phosphorylation
Myofibroblasts
Ventricular remodeling
Cells
Cultured
Cell Proliferation
Ventricular Remodeling
biology
business.industry
Myocardium
Receptor
Transforming Growth Factor-beta Type II
Cardiovascular Agents
Cell Differentiation
Recovery of Function
General Medicine
Transforming growth factor beta
medicine.disease
Immunohistochemistry
Actins
Rats
Disease Models
Animal
Endocrinology
Animals
Newborn
biology.protein
Myocardial fibrosis
Cardiology and Cardiovascular Medicine
business
Receptors
Transforming Growth Factor beta
Myofibroblast
Transforming growth factor
Zdroj: Coronary Artery Disease. 21:369-377
ISSN: 0954-6928
Popis: 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
Databáze: OpenAIRE
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