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To investigate the mechanism and thesignificance of TGR in modulating the expression ofPlatelet-Derived Growth Factor Receptor-α (PDGFR-α)in human osteoblasts. Methods The osteoblasts were isolated from humanfetal calvaria. The percentage of cell increase (PCI) inevery 4 hours was calculated to demonstrate theproliferation of osteoblasts affected by PDGF-AA andTGFβ. The osteoblasts were cultured with TGFβ for 24hours and with PDGF-AA for another 24 hours, and thecells proliferation was shown by PCI too. Theosteoblasts were cultured with TGFβfor 24 h, and thePDGFR-α of the cells were measured byimmunofluorescent analysis. Results PCI was increased by 48.2% and 22.4%after PDGF-AA and TGFβ were added into the mediumfor 24 hours respectively (P < 0.05 ), and PCIdecreased after the removal of the two cytokines.Preincubated with TGFβfor 24 hours and thenstimulated with PDGF-AA, PCI grew slowly. TGFβdownregulated the expression of the PDGFR-a. Conclusion TGFβ can downregulate the mitogenesisof PDGF-AA by lowering the number of PDGFR-α.
To investigate the mechanism and the signature of TGR in modulating the expression of Platelet-Derived Growth Factor Receptor-α (PDGFR-α) in human osteoblasts. Methods The osteoblasts were isolated from human calvaria. The percentage of cell increase (PCI) inevery 4 hours was calculated to demonstrate the protoliferation of osteoblasts affected by PDGF-AA and TGFβ. The osteoblasts were cultured with TGFβ for 24hours and with PDGF-AA for another 24 hours, and the cells proliferation was shown by PCI too. Theosteoblasts were cultured with TGFβfor 24 h, and the PDGFR -α of the cells were measured by immunofluorescent analysis. Results PCI was increased by 48.2% and 22.4% after PDGF-AA and TGFβ were added into the medium for 24 hours respectively (P <0.05), and PCIdecreased after the removal of the two cytokines. Preincubated with TGFβ for 24 hours and the inspired with PDGF-AA, TGFαdownregulated the expression of the PDGFR-a. Conclusion TGFβ ca n downregulate the mitogenesis of PDGF-AA by lowering the number of PDGFR-α.