Modulatory effect of 1,25-dihydroxyvitamin D 3 on IL1 β -induced RANKL, OPG, TNF α , and IL-6 expression in human rheumatoid synoviocyte MH7A.
Modulatory effect of 1,25-dihydroxyvitamin D 3 on IL1 β -induced RANKL, OPG, TNF α , and IL-6 expression in human rheumatoid synoviocyte MH7A.
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DOI：
10.1155/2013/160123
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发表时间：
2013
影响因子：
--
通讯作者：
Tan W
中科院分区：
文献类型：
--
作者：
Feng X;Lv C;Wang F;Gan K;Zhang M;Tan W
核因子受体激活剂κB配体(RANKL)通过促进破骨细胞生成，在类风湿关节炎(RA)的骨侵蚀中发挥重要作用。鉴于1，25(OH)2D3已被认为是RANKL表达的有效诱导剂，补充维生素D是否会导致RANKL的过度表达，从而促进RA的过度破骨细胞形成和骨吸收，应该得到澄清。在此，我们研究了1，25(OH)2D3对人类风湿滑膜细胞MH7A炎症状态下RANKL及其诱骗受体OPG表达的调节作用。用IL-1β刺激MH7A细胞，然后用不同浓度的1，25(OH)2D3处理48 h，与不加1，25(OH)2D3的MH7A细胞相比，IL-1β诱导的MH7A细胞的OPG/RANKL比值显著升高，IL-6和TMNKLβ表达水平显著降低，IL-6蛋白表达显著降低。当1，25(OH)2D3和IL1β同时作用于RAW264.7细胞时，破骨细胞的形成明显减少。综上所述，尽管1，25(OH)2D3具有诱导RANKL表达的生物学功能，但它可以上调OPG/RANKL比值，并在滑膜细胞炎症环境中介导抗炎作用，从而有助于抑制炎症诱导的RA破骨细胞的形成。
Receptor activator of nuclear factor κB ligand (RANKL) plays a crucial role in the bone erosion of rheumatoid arthritis (RA) by prompting osteoclastogenesis. Considering that 1,25(OH)2D3 has been suggested as a potent inducer of RANKL expression, it should clarify whether vitamin D supplement could result in RANKL overexpression and thereby facilitate excessive osteoclastogenesis and bone resorption in RA. Here, we investigated modulatory effect of 1,25(OH)2D3 on the expression of RANKL and its decoy receptor osteoprotegerin (OPG) in an inflammatory condition of human rheumatoid synoviocyte MH7A. MH7A cells were stimulated with IL1β and then treated with different concentrations of 1,25(OH)2D3 for 48 h. A significantly elevated OPG/RANKL ratio and markedly decreased levels of IL-6 and TNFβ mRNA expression in cells and IL-6 protein in supernatants were observed in IL1β-induced MH7A in the presence of 1,25(OH)2D3 compared with those in the absence of it. Osteoclast formation was obviously decreased when RAW264.7 cells were treated with both 1,25(OH)2D3 and IL1β. In summary, although it has a biological function to induce RANKL expression, 1,25(OH)2D3 could upregulate OPG/RANKL ratio and mediate anti-inflammatory action in an inflammatory milieu of synoviocyte, contributing to the inhibition of inflammation-induced osteoclastogenesis in RA.
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