Effect of Tumor Growth Factor-β on Osteogenesis in Osteoporosis Rats by Regulating Bone Morphogenetic Protein Signaling Pathway
The balance of osteoblasts and osteoclasts is critical for bone formation and remodeling and imbalance causes osteoporosis (OP). TGF-β regulates bone tissue repair and regeneration, but TGF-β’s role in osteogenesis in OP has not been elucidated. OVX-induced OP rat models were constructed and rat BMSCs were isolated and assigned into control group, OP group, and TGF-β group (transfected with TGF-β1 plasmid followed by analysis of cell proliferation by MTT assay, RUNX2 and OPN expression by Real time PCR, ALP activity and secretion of TGF-β, BMP-2 and BMP-9 by ELISA. In addition, RANKL was added to induce BMSCs differentiation into to osteoclasts which were transfected with TGF-β1 followed by analysis of cell proliferation, c-Fos and TRAP expression and secretion of BMP-2 and BMP-9. OP group rats had significantly reduced secretion of TGF-β1, BMP-2 and BMP-9, reduced cell proliferation, decreased RUNX2 and OPN expression and ALP activity (P <0.05). Transfection of TGF-β1 in BMSCs of OP group rats could significantly reverse the above changes (P <0.05). TGF-β1 significantly inhibited osteoclast proliferation, decreased expression of c-Fos and TRAP, and increased secretion of BMP-2 and BMP-9 (P <0.05). TGF-β1 level in OP is decreased. Up-regulating TGF-β promotes osteoblast differentiation in OP rats by regulating BMP signaling pathway, and inhibits osteoclast proliferation and differentiation.