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Abstract Title:

Melatonin reversed TNFα-inhibited osteogenesis of human MSCs by stabilizing SMAD1 protein.

Abstract Source:

J Pineal Res. 2016 Jun 6. Epub 2016 Jun 6. PMID: 27265199

Abstract Author(s):

Chengjie Lian, Zizhao Wu, Bo Gao, Yan Peng, Anjing Liang, Caixia Xu, Lei Liu, Xianjian Qiu, Junjun Huang, Hang Zhou, Yifeng Cai, Peiqiang Su, Dongsheng Huang

Article Affiliation:

Chengjie Lian

Abstract:

TNFα plays a pivotal role in inflammation-related osteoporosis through the promotion of bone resorption and suppression of bone formation. Numerous drugs have been produced to treat osteoporosis by inhibiting bone resorption, but they offer few benefits to bone formation, which is what is needed by patients with severe bone loss. Melatonin, which can exert both anti-inflammatory and pro-osteogenic effects, shows promise in overcoming TNFα-inhibited osteogenesis and deserves further research. The current study demonstrated that melatonin rescued TNFα-inhibited osteogenesis of human MSCs and that the interactions between SMURF1 and SMAD1 mediated the crosstalk between melatonin signaling and TNFα signaling. Additionally, melatonin treatment was found to down-regulate TNFα-induced SMURF1 expression and then decrease SMURF1-mediated ubiquitination and degradation of SMAD1 protein, leadingto steady BMP-SMAD1 signaling activity and restoration of TNFα-impaired osteogenesis. Thus, melatonin has prospects for treating osteoporosis caused by inflammatory factors due to its multifaceted functions on regulation of bone formation, bone resorption, and inflammation. Further studies will focus on unveiling the specific mechanisms by which melatonin down-regulates SMURF1 expression and confirming the clinical therapeutic value of melatonin in the prevention and therapy of bone loss associated with inflammation. This article is protected by copyright. All rights reserved.

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