Cellular transplant applied with rat bone marrow stromal cells preconditioned with stromal-derived factor 1 to treat acute myocardial infarction
10.3760/cma.j.issn.0254-1785.2009.06.012
- VernacularTitle:大鼠骨髓间充质细胞经SDF-1预处理后移植对急性心肌梗死的治疗效果
- Author:
Jun CHEN
;
Kailun ZHANG
;
Xinling DU
- Publication Type:Journal Article
- Keywords:
Mesenchymal stem cells;
Ischemic preconditioning;
Myocardial infarction;
Cell transplantation
- From:
Chinese Journal of Organ Transplantation
2009;30(6):362-365
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of preconditioning (PC) with stromal-derived factor 1 alpha (SDF-1) on the levels of apoptosis of bone marrow stromal cells (BMSC) treated with hypoxia plus serum deprivation, and observe the therapeutic efficacy of cellular transplant with BMSC preconditioned with SDF-1 in rats with acute myocardial infarction. Methods BMSC were cultured with the whole marrow-adherence way. RT-PCR and immunohistochemistry were used to determine the expression of CXCR4. BMSC were incubated in medium for 24 h with 10 and 100 μg/L SDF-1 respectively, then treated with hypoxia plus serum deprivation for 6 h. The levels of apoptosis were detected by flow cytometry and TUNEL method. Acute myocardial infarction (AMI) model was established in SD rats, and BMSC preconditioned or non-preconditioned with SDF-1 were transplanted into border zone around infarct area, then heart function was measured after two weeks by ultrasonography. Results BMSC exhibited the CXCR4 expression. The number of apoptotic cells was significantly reduced in SDF-1 PC group than in control group (P<0.05), and 100μg/L SDF-1 PC group had the lowest level of apoptosis. AMI model was established successfully. Two weeks after BMSC transplant, significant improvement in cardiac function was observed in 100 μg/L SDF-1 PC group as compared with the non-PC group (P<0.05). Conclusions PC with the chemokine SDF-1 suppresses the apoptosis of BMSC treated with hypoxia plus serum deprivation. SDF-1 PC is a novel approach for enhancing therapeutic efficacy of cellular transplant in rats with AML
