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The Effect Of Recombinant Adenovirus Vector Expressing Soluble TGF-β Type Ⅱ Receptor On Ventricular Remodeling After Myocardial Infarction In Rats

Posted on:2012-12-10Degree:MasterType:Thesis
Country:ChinaCandidate:L L ZhangFull Text:PDF
GTID:2154330335486658Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To observe the effect of recombinant adenovirus vector expressing the extracellular domain gene of transforming gowth factor-βtypeⅡreceptor ( pAd-sTGFβRⅡ) transfection on ventricular remodeling after myocardial infarction (MI) in rats, and explore the possible mechanisms.Methods: MI was induced in Sprague-Dawley (SD) rats by ligating the anterior descending of left coronary artery, the rats surviving to the third day after MI were entered into the study, randomly divided into MI group, pAd-sTGFβRⅡgroup, vector group, and the sham group were used as control. After four weeks, the expression of sTGFβRⅡgene was observed under fluorescence microscope by frozen tissue sections, myocardium tissue structure by HE staining and typeⅠandⅢcollagen expression by Sirius red-saturated picric acid staining. The expressions ofα-smooth muscle actin (α-SMA) and matrix metalloproteinase-9 (MMP-9) protein were determined by immunohistochemical method, and apoptosis-related genes bax and bcl-2 mRNA by RT-PCR.Results: (1) Compared with MI group, the expression of typeⅠandⅢcollagen , MMP-9 protein, bax mRNA and the number ofα-SMA positive cells decreased significantly (P<0.01), and bcl-2 mRNA expression increased (P<0.01) in pAd-sTGFβRⅡgroup. (2) Compared with the sham group, the expression of typeⅠandⅢcollagen , MMP-9 protein and bax mRNA increased (P<0.01), and bcl-2 mRNA expression had no significant difference in pAd-sTGFβRⅡgroup .Conclusion: The pAd-sTGFβRⅡintervention may mitigate ventricular remodeling after MI by a potential mechanism of inhibiting myocardial fibrosis and cardiomyocyte apoptosis mediated by TGF-β.
Keywords/Search Tags:myocardial infarction, soluble transforming growth factor-βtypeⅡreceptor, ventricle remodeling, role mechanisms
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