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首页> 外文期刊>Journal of Cellular Physiology >TNF-alpha promotes osteoclastogenesis through JNK signaling-dependent induction of Semaphorin3D expression in estrogen-deficiency induced osteoporosis
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TNF-alpha promotes osteoclastogenesis through JNK signaling-dependent induction of Semaphorin3D expression in estrogen-deficiency induced osteoporosis

机译：tnf促进osteoclastogenesis通过物signaling-dependent诱导Semaphorin3D表达estrogen-deficiency诱导骨质疏松症

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摘要

Tumor necrosis factor a (TNF-alpha)-induced osteoclast formation have been demonstrated to play an important role in the pathogenesis of estrogen deficiency-mediated bone loss, but the exact mechanisms by which TNF-alpha enhanced osteoclast differentiation were not fully elucidated. The class III semaphorins members were critical to regulate bone homeostasis. Here, we identified a novel mechanism whereby TNF-alpha increasing Semaphorin 3D expression contributes to estrogen deficiency-induced osteoporosis. In this study, we found that Semaphorin 3D expression was upregulated by TNF-alpha during the process of RANKL-induced osteoclast differentiation. Inhibition of Semaphorin 3D in pre-osteoclasts could attenuate the stimulatory effects of TNF-alpha on osteoclast proliferation and differentiation. Mechanistically, blocking of the Jun N-terminal kinase (JNK) signaling markedly rescued TNF-alpha-induced Semaphorin 3D expression, suggesting that JNK signaling was involved in the regulation of Semaphorin 3D expression by TNF-alpha. In addition, silencing of Semaphorin 3D in vivo could alleviate estrogen deficiency-induced osteoporosis. Our results revealed a novel function for Semaphorin 3D and suggested that increased Semaphorin 3D may contribute to enhanced bone loss by increased TNF-alpha in estrogen deficiency-induced osteoporosis. Thus, Semaphorin 3D may provide a potential therapeutic target for the treatment of estrogen-deficiency induced osteoporosis.
机译：全身的肿瘤坏死因子(tnf)破骨细胞形成已经证明的发病机制中扮演重要角色雌激素deficiency-mediated骨质流失,但确切机制tnf增强破骨细胞分化不完全阐明。调节骨体内平衡是至关重要的。我们发现了一个新的机制tnf增加Semaphorin 3 d表达式的贡献雌激素deficiency-induced骨质疏松症。这项研究中,我们发现Semaphorin 3 d期间,tnf表达调节RANKL-induced破骨细胞的过程分化。pre-osteoclasts可以减弱刺激tnf对破骨细胞增殖的影响和分化。小君n端激酶(物)的信号明显获救TNF-alpha-induced Semaphorin 3 d表达式,表明物信号参与Semaphorin 3 d的规定tnf表达。Semaphorin 3 d体内可以缓解雌激素deficiency-induced骨质疏松症。揭示了小说Semaphorin 3 d和函数建议增加Semaphorin 3 d有助于增强骨质流失增加tnf在雌激素deficiency-induced骨质疏松症。潜在的治疗目标治疗estrogen-deficiency诱导骨质疏松症。

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