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首页> 外文期刊>Archives of Oral Biology >Osteogenic induction and 1,25-dihydroxyvitamin D3 oppositely regulate the proliferation and expression of RANKL and the vitamin D receptor of human periodontal ligament cells.
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Osteogenic induction and 1,25-dihydroxyvitamin D3 oppositely regulate the proliferation and expression of RANKL and the vitamin D receptor of human periodontal ligament cells.

机译:成骨诱导和1,25-二羟基维生素D3反向调节人牙周膜细胞的RANKL和维生素D受体的增殖和表达。

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OBJECTIVE: Human periodontal ligament cells (hPDLCs) may play an important role in osteoclastogenesis in alveolar bone by expressing the receptor activator of NF-KappaB ligand (RANKL) and osteoprotegerin (OPG). The present study aimed to investigate the differences between the effects of osteogenic induction and 1,25-dihydroxyvitamin D(3) (VD(3)) on hPDLC proliferation and the expression of RANKL, osteoprotegerin, and the vitamin D receptor (VDR) in hPDLCs. METHODS: Primary cultures of 11 hPDLC populations from 11 donors were obtained. Three samples of each hPDLC population from passage 3 were, respectively, treated with osteogenic induction medium, 10(-8)M VD(3), or vehicle as a control. Cell proliferation at days 0, 1, 3, 5, and 7 was estimated with the MTT method. At day 6, the mRNA levels of RANKL, OPG and VDR were determined with real-time RT-PCR. RESULTS: Osteogenic induction significantly promoted hPDLC proliferation, while VD(3) inhibited proliferation. Osteogenic induction significantly down-regulated the mRNA level of RANKL by 1.61-fold (P = 0.033) and decreased the level of VDR by 2.13-fold (P = 0.003), while there was no change in the level of OPG and OPG/RANKL ratio with osteogenic induction. On the contrary, VD(3) significantly up-regulated the level of RANKL by 9.58-fold (P = 0.001) and increased the level of VDR by 3.15-fold (P = 0.004), while down-regulating the OPG/RANKL ratio by 7.14-fold (P=0.004). CONCLUSION: Osteogenic induction and VD(3) exert opposite effects in regulating hPDLC proliferation and mRNA expression of RANKL and VDR. This may induce hPDLCs to play different roles in alveolar bone metabolism.
机译:目的:人牙周膜细胞(hPDLC)可能通过表达NF-κB配体(RANKL)和骨保护素(OPG)的受体激活剂在牙槽骨的破骨细胞形成中发挥重要作用。本研究旨在探讨成骨诱导和1,25-二羟基维生素D(3)(VD(3))对hPDLC增殖的影响以及RANKL,骨保护素和维生素D受体(VDR)的表达之间的差异。 hPDLC。方法:获得了来自11个供体的11个hPDLC人群的原代培养。来自第3代的每个hPDLC群体的三个样品分别用成骨诱导培养基,10(-8)M VD(3)或媒介作为对照进行处理。用MTT法估计在第0、1、3、5和7天的细胞增殖。在第6天,通过实时RT-PCR测定RANKL,OPG和VDR的mRNA水平。结果:成骨诱导显着促进hPDLC增殖,而VD(3)抑制增殖。成骨诱导显着下调RANKL的mRNA水平1.61倍(P = 0.033),降低VDR水平2.13倍(P = 0.003),而OPG和OPG / RANKL的水平没有变化成骨诱导的比例。相反,VD(3)显着上调RANKL的水平9.85倍(P = 0.001),将VDR的水平上调3.15倍(P = 0.004),同时下调OPG / RANKL比减少7.14倍(P = 0.004)。结论:成骨诱导和VD(3)在调节hPDLC增殖以及RANKL和VDR的mRNA表达方面起相反的作用。这可能会诱导hPDLC在牙槽骨代谢中发挥不同的作用。

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