白细胞介素-6与前列腺素E2通过骨保护素/核因子κB受体活化因子配体/核因子κB受体活化因子系统对破骨细胞生成的交互作用。
Interactive effect of interleukin-6 and prostaglandin E2 on osteoclastogenesis via the OPG/RANKL/RANK system.
作者信息
Liu Xin-Hua, Kirschenbaum Alexander, Yao Shen, Levine Alice C
机构信息
Department of Medicine, Box 1055, Mount Sinai School of Medicine, New York, NY 10029.
出版信息
Ann N Y Acad Sci. 2006 Apr;1068:225-33. doi: 10.1196/annals.1346.047.
The OPG/RANKL/RANK system regulates osteoclastogenesis. Both cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and interleukin-6 (IL-6) are reported to induce osteoclast differentiation. The mechanisms underlying these signaling pathways on the OPG/RANKL/RANK system are not fully understood. We herein demonstrate that COX-2 and PGE2 stimulated osteoclastogenesis through inhibition of OPG secretion, stimulation of RANKL production by osteoblasts, and upregulation of RANK expression in osteoclasts. PGE2 also stimulated IL-6 production, and IL-6, in turn, increased PGE2 secretion, COX-2, and EP4/EP2 expression in bone cells. These findings provide evidence of interactive effect of PGE2 and IL-6 signaling pathways in osteoclastogenesis via effect on the OPG/RANKL/RANK system.
骨保护素/核因子κB受体活化因子配体/核因子κB受体活化因子（OPG/RANKL/RANK）系统调节破骨细胞生成。据报道，环氧合酶-2（COX-2）/前列腺素E2（PGE2）和白细胞介素-6（IL-6）均可诱导破骨细胞分化。这些信号通路作用于OPG/RANKL/RANK系统的潜在机制尚未完全阐明。我们在此证明，COX-2和PGE2通过抑制OPG分泌、刺激成骨细胞产生RANKL以及上调破骨细胞中RANK的表达来刺激破骨细胞生成。PGE2还刺激IL-6的产生，而IL-6反过来又增加骨细胞中PGE2的分泌、COX-2以及EP4/EP2的表达。这些发现为PGE2和IL-6信号通路通过影响OPG/RANKL/RANK系统在破骨细胞生成中存在交互作用提供了证据。
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