Background
The expression of miRNA-21 was high in cells that were derived from MSCs, but, the role of miRNA-21in the MSCs was unknown. Material/
Conclusions
The results also suggested that, the up-regulation of miRNA-21 enhanced proliferation of MSCs, reducing the apoptosis of MSCs. MiRNA-21 promotes the differentiation of MSCs, which may pave the way for the treatment directed toward restoring miRNA-21 function for myocardial ischemia.
Methods
In this study, flow cytometry, which was used to identify the surface-associated antigens of MSCs. The 10 μmol/l 5-azacytidine was used to induce MSCs to differentiate to cardiomyocyte-like cells. Immunofluorescence, that was for detected the expression of troponin I (cTnI). The samples were assigned to 3 groups: the blank group, the miRNA-21 mimic group, and the negative control (NC) group. The proliferation of MSCs was detected by methyl thiazolylte-trazolium (MTT), the apoptosis of MSCs was analyzed by flow cytometry, Western-blot, which was used to identify the expression of cTNI and myoD in the MSCs.
Results
The proliferation of MSCs was increased, because of the over expression of miRNA-21; But, the apoptotic rate of the MSCs were slower in MIRNA-21 group, on account of the expression of miRNA-21 was higher than that of in the NC and CK groups. The expression of cTNI in miRNA-21 group was higher than that of in the NC and CK groups. Conclusions: The results also suggested that, the up-regulation of miRNA-21 enhanced proliferation of MSCs, reducing the apoptosis of MSCs. MiRNA-21 promotes the differentiation of MSCs, which may pave the way for the treatment directed toward restoring miRNA-21 function for myocardial ischemia.