BMP9 overexpressing adipose-derived mesenchymal stem cells promote cartilage repair in osteoarthritis-affected knee joint via the Notch1/Jagged1 signaling pathway.

Osteoarthritis (OS) is a common disease in orthopedics. Although OS is known as an inflammation mediated by inflammatory cytokines; however, the mechanism is poorly understood. In the present study, the role of bone morphogenetic protein-9 (BMP9) was investigated in chondrogenic differentiation of adipose-derived mesenchymal stem cells (ADMSCs). ADMSCs were transfected with BMP9. BMP9 mRNA expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Type II collagen and aggrecan expression was detected by western blotting and RT-qPCR. Mouse models of knee OS were established. Hematoxylin-eosin staining and toluidine blue staining were performed to observe changes in the OS-affected knee joint. After intra-articular injection of ADMSCs transfected with BMP9, intra-articular expression of type II collagen and aggrecan was detected by western blot analysis and RT-qPCR. After the Notch signaling pathway was inhibited in ADMSCs, ADMSCs were injected into the articular cavity. The expression of Notch signaling pathway-related proteins Notch1 and Jagged1 was detected by western blot analysis and RT-qPCR. BMP9 promoted chondrogenic differentiation of ADMSCs. After injection of BMP9 overexpressing ADMSCs into the articular space, type II collagen and aggrecan expression was increased. When the Notch signaling pathway of ADMSCs was inhibited, the ability of BMP9 overexpressing ADMSCs to repair the cartilage in the OS-affected knee joint was attenuated. These results demonstrate that upregulating BMP9 protein expression may promote the chondrogenic differentiation of ADMSCs. Intra-articular injection of ADMSCs contributes to cartilage repair in OS-affected knee joints through the Notch1/Jagged1 signaling pathway.