Effect of 1,25-Dihydroxyvitamin Don Bone Marrow Mesenchymal Stem Cells Differentiation and Osteoporosis Through Wingless-Related Integration Site 5 (Wnt5)/Tumor Growth Factor-β TGF-β Signaling Pathway

Osteoporosis (OP) is a common clinical geriatric disease. Bone marrow mesenchymal stem cells (BMSCs) are widely applied in bone engineering. 1,25-dihydroxyvitamin D (1,25-(OH) 2D) deficiency involves in geriatric disease. However, its effects on BMSCs differentiation and osteoporosis have not yet been elucidated. An OVX-induced OP rat model was constructed and treated with 10 mu M 1,25-(OH) 2D followed by analysis of bone mineral density and ALP activity. Rat BMSCs were isolated and divided into control group, OP group, OP rat BMSCs, and VD group (OP rats were injected with 1 mu M 1,25-(OH) 2D) followed by analysis of cell survival by MTT assay, Caspase 3 activity, type I collagen and Osterix expression by Real time PCR, Wnt5 expression by Western blot and TGF-beta secretion by ELISA. The bone density and ALP activity was significantly decreased in OP rats (P < 0.05). 1,25 (OH) 20 injected into OP rats significantly increased bone density and ALP activity (P < 0.05). The survival rate of BMSCs in OP group was significantly decreased and Caspase 3 activity was increased along with downregulated type I collagen and Osterix, TGF-beta secretion and Wnt5 expression (P < 0.05). Adding 1,25-(OH) 2D to BMSCs cells in OP group could significantly reverse the above changes (P < 0.05). 1,25-dihydroxyvitamin D promotes BMSCs proliferation by regulating Wnt5/TGF-beta signaling, promotes differentiation into osteogenesis, increases bone density, and then improves osteoporosis.