Abstract
OBJECTIVE: The aim of this study was to investigate the molecular mechanism of TGF-β1 in regulating chondrocyte proliferation through MSC-exosomes. METHODS: An osteoarthritis (OA) rat model was established. Cartilage degradation was quantified by using OARSI score. TGF-β1 was used to stimulate MSCs. The expressions of miR-135b and Sp1 in MSCs, MSC-exosomes and C5.18 cells were detected. The cell viability of C5.18 cells was measured using MTT assay. RESULTS: TGF-β1 stimulation enhanced miR-135b expression in MSC-exosomes, and MSC-exosomes derived miR-135b increased the cell viability of C5.18 cells. Moreover, miR-135b negatively regulated Sp1 expression. The cell viability of C5.18 cells in TGF-β1+miR-135b inhibitor+si-control group was reduced, while the cell viability in TGF-β1+miR-135b inhibitor+si-Sp1 group was enhanced. In rat experiments, OARSI score was decreased and the number of chondrocytes was increased in OA+TGF-β1+MSC-exosome group, while the score and the number had an opposite trend in OA+TGF-β1+MSC-miR135b inhibitor-exosome group. CONCLUSION: TGF-β1 promoted chondrocyte proliferation by regulating Sp1 through MSC-exosomes derived miR-135b, then promoted cartilage repair.