Effects of mesonchymal stem cells modified by human heine oxygenase-I gene on cardiac inflammatory cytokine and the ventricular remodeling
- VernacularTitle:血红素氧合酶-1修饰骨髓间充质干细胞对大鼠梗死心肌炎症细胞因子及心室重构的影响
- Author:
Bin ZENG
;
Guosheng LIN
;
Hong JIANG
;
Bo YANG
- Publication Type:Journal Article
- Keywords:
Mesenchymal stem coils;
Cell transplantation;
Cytokines;
Inflammatory;
Acute myocardialinfarction
- From:
Chinese Journal of Emergency Medicine
2008;17(8):825-829
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of mesenchymul stem cells(MSCs) transfected with human home oxygenase- 1 gene on the inflammatory cytokines and the ventricular remodeling after myocardial infarction in rats.Method MSCs were acquired from the hone marrow of adults rats.They were isolated,purified cultured,and transfected with Adv-HO-1,or Adv-GFP in vitro before transplantation.At 1 hours after left coronary artery ligation,Adv-HO-1-MSCs or Adv-GFP-MSCs marked with DAPI were directly injected into the horder of cardiac infarction in rats.At 4 days after transplantation,western blot analysis was used to measure HO-1 protein expression in the the horder of cardiac infarction.The levels of VEGF,bFGF,HGF protein expression were measured by ELISA,and the levels of TNF-α,IL-1β,IL-6,IL-10 mRNA expression were measured by RT-PCR.The rat heart function was measured by echocardiography.At 4 weeks after transplantation,ventricular remodeling and pathological changes were measured by HE and Masson staining.Results The Adv-HO-1-MSCa treated group showed marked increase of HO-1 rotein (P<0.05),and displayed significant increase of montioned cytokines above,P <0.05,compared with other groups.The Adv-HO-1-MSCs treated group displayed significant reduction of mRNAs expreesion of TNF-α,IL-1β,IL-6,and significant increase in IL-10 mRNA expression,with P<0.05,compared with others.Conclusions HO-1-MSCs could secrete multiple cytokines in infarction hearts,and had beneficial effects on inflammatory cytokines,remodeling processes and cardiac function.
