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Lanthanum Chloride Attenuates Osteoclast Formation and Function Via the Downregulation of Rankl‐Induced Nf‐κb and Nfatc1 Activities
Author(s) -
Jiang Chuan,
Shang Jiangyinzi,
Li Zhe,
Qin An,
Ouyang Zhengxiao,
Qu Xinhua,
Li Haowei,
Tian Bo,
Wang Wengang,
Wu Chuanlong,
Wang Jinwu,
Dai Min
Publication year - 2016
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25065
Subject(s) - rankl , osteoclast , osteolysis , chemistry , bone resorption , downregulation and upregulation , osteoblast , microbiology and biotechnology , nf κb , in vivo , cathepsin k , endocrinology , medicine , receptor , signal transduction , activator (genetics) , in vitro , biochemistry , biology , gene , surgery
The biological activities of lanthanum chloride (LaCl 3 ) and the molecular mechanisms of action underlying its anti‐inflammatory, anti‐hyperphosphatemic, and osteoblast‐enhancing effects have been studied previously, but less is known about the effects of LaCl 3 on osteoclasts. The present study used in vivo and in vitro approaches to explore the effects of LaCl 3 on osteoclasts and osteolysis. The results indicated that LaCl 3 concentrations that were non‐cytotoxic to mouse bone marrow‐derived monocytes attenuated receptor activator of nuclear factor‐κB ligand (RANKL)‐stimulated osteoclastogenesis, bone resorption, mRNA expression of osteoclastogenic genes in these cells, including cathepsin K, calcitonin receptor, and tartrate‐resistant acid phosphatase (TRAP). Further, LaCl 3 inhibited RANKL‐mediated activation of the nuclear factor‐κB (NF‐κB) signaling pathway, and downregulated mRNA and protein levels of nuclear factor of activated T‐cells, cytoplasmic, calcineurin‐dependent 1 (NFATc1), and c‐fos. In vivo, LaCl 3 attenuated titanium (Ti) particle‐induced bone loss in a murine calvarial osteolysis model. Histological analyses revealed that LaCl 3 ameliorated bone destruction and decreased the number of TRAP‐positive osteoclasts in this model. These results demonstrated that LaCl 3 inhibited osteoclast formation, function, and osteoclast‐specific gene expression in vitro, and attenuated Ti particle‐induced mouse calvarial osteolysis in vivo, where the inhibition of NF‐κB signaling and downregulation of NFATc1 and c‐fos played an important role. J. Cell. Physiol. 230: 142–151, 2016. © 2015 Wiley Periodicals, Inc.