MicroRNA-564 Promotes The Proliferation And Differ-Entiation Of Synovial Mesenchymal Stem Cells Into Chondrocytes By Targeting Transforming Growth Factor Beta 1

Objective:In the process of articular cartilage defect repair,multiple miRNAs are involved in the process of cartilage formation of synovial mesenchymal stem cells(SMSCs);we investigated the role of miR-564 in promoting the proliferation and differentiation of synovial mesenchymal stem cells(SMSCs)to chondrocytes.Methods:The third generation of SMSCs were used as experimental cells.The experimental design was as follows:the blank group of SMSCs;the control group of miRNA inhibitor transfected with SMSCs;the experimental group of miR-564 inhibitor transfected into SMSCs.Three groups of SMSCs were cultured in chondrocytes for 21 days.The histomorphology of chondrocytes was observed and the three cell proliferation curves were detected within 7 days before induction,and the cartilage differentiation-specific genes and proteins(Collagen,proteoglycan,SOX9,TGF??1Smad4)in the three groups of SMSCs were detected,Finally,the chondrogenic effect of miR-564 was examined after blocking the target gene TGF-?1.Results:1.The morphology and characteristics of the cells were consistent with chondrocytes,and the number of cells in experimental group was more and the blue staining was more obvious;2.The cell proliferation curve showed that the proliferation rate of the experimental group was significantly faster than that of the control group(F=0.842,P<0.01);3.The expression of genes and proteins related to chondrocyte differentiation was significantly increased with in experimental group(F=2274.75;F=447.31;F=30476.22;P<0.01);and the key genes and proteins of TGF?-BMP signaling pathway(TGF-BMP)increased significantly in the experimental group(F=457.02,F=291.19;P<0.01).4.The relative expression of genes related to cartilage differentiation decreased after blocking TGF-?1(t=6.08,t=18.64,t=97.24,P<0.01;P<0.01).Conclusion:The downregulation mediated by miR-564 can promote the differentiation and proliferation of SMSCs into chondrocytes by targeting TGF-?1.