Résumé
Objective: To verify the hypothesis that cells with characteristics similar to bone marrow mesenchymal stem cells(MSCs) can be isolated and cultured from human fetal articular cartilage. Methods: Human fetal articular cartilages were harvested from fetuses aborted between 12 and 20 weeks. Cells were grown in monolayer cultures in IMDM medium containing antibiotics, L-glutamine and fetal calf serum. Cells were induced to differentiate into adipocytes, osteoblasts, chondrocytes, and neurons. At various time points, parental and passaged cells were subjected to FACS analysis to determine cell phenotype. Results: We successfully isolated and cultured MSCs from human fetal articular cartilage. These cells had the same morphology, phenotype, and ability to differentiate in vitro as MSCs of bone marrow origin. Conclusion: This study shows that cells with characteristics of MSCs can be isolated and cultured from human fetal articular cartilage.
Résumé
Objective:To clarify the role of Heat shock proteins (HSPs) on the cardiac function during acute myocardial infarction (AMI) after bone marrow cell implantation (BMT), we examined the expression of HSP32 and HSP70 in a rat model of myocardial infarction. Methods: Myocardial infarction model was induced in the inbred Lewis rats by left anterior descending artery ligation,and 5?10 6 of bone marrow mononuclear cells (BM MNCs) were injected into an ischemic zone. On days 1, 3, 7 and 14 post infarct, the differentiations of transplanted cells and the expressions of HSP32 and HSP70 were determined by immunofluorescence or RT-PCR. The cardiac function was evaluated by echocardiography. Results: Immunofluorescence microscopy of hearts from BMT group revealed that expressions of HSP32 and HSP70 were promoted within cardiomyocytes in the infarction zone and the peri infarct zone,and expressed within some transplanted bone marrow cells as well. RT-PCR also showed the mRNA expression levels of HSP32 and HSP70 in BMT group were significantly higher than those of the control group, peaked on day 3 post infarct (5.0 fold and 2.9 fold, respectively, P