期刊
CELL COMMUNICATION AND SIGNALING
卷 17, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12964-019-0442-3
关键词
Osteoclasts; T007; Peroxisome proliferator-activated receptor-gamma; Osteoporosis; Receptor activator of nuclear factor-kappa B ligand
类别
资金
- National Key R&D Program of China [2018YFC1105200]
- Key Research and Development Plan in Zhejiang Province [2018C03060]
- Natural Science Fund of Zhejiang Province [LY18H060001]
- National Nature Science Fund of China [81772387, 81601925]
Background Osteoclasts are key determinant cellular components implicated in the development and progression of disorders driven by bone damage. Herein, we studied the upshot of T007, an antagonist of peroxisome proliferator-activated receptor-gamma (PPAR gamma), on osteoclastogenesis using cell and animal models. Results The in vitro assays revealed that T007 hindered the osteoclastogenesis caused by the treatment with the receptor activator of nuclear factor-kappa B ligand (RANKL) through inhibiting the levels of PPAR gamma in cells. The PPAR gamma siRNA partially reproduced the inhibitory action of T007. The opposite findings were produced after PPAR gamma overexpression. Furthermore, T007 prevented from bone loss in a mouse model of osteoporosis induced by ovariectomy (OVX). These findings implied that T007 is a potential efficient drug for the prophylaxis and cure of osteoclast-related disorders. Conclusions Taken together, our findings demonstrated that T007 impedes osteoclastogenesis and will be useful for the therapy of bone related diseases, essentially osteoporosis.
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