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http://dx.doi.org/10.14348/molcells.2015.2241

MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation  

Kim, Kabsun (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Kim, Jung Ha (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Kim, Inyoung (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Lee, Jongwon (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Seong, Semun (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Park, Yong-Wook (Department of Rheumatology, Chonnam National University Medical School and Hospital)
Kim, Nacksung (Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School)
Publication Information
Molecules and Cells / v.38, no.1, 2015 , pp. 75-80 More about this Journal
Abstract
Osteoclasts are unique cells responsible for the resorption of bone matrix. MicroRNAs (miRNAs) are involved in the regulation of a wide range of physiological processes. Here, we examined the role of miR-26a in RANKL-induced osteoclastogenesis. The expression of miR-26a was upregulated by RANKL at the late stage of osteoclastogenesis. Ectopic expression of an miR-26a mimic in osteoclast precursor cells attenuated osteoclast formation, actin-ring formation, and bone resorption by suppressing the expression of connective tissue growth factor/CCN family 2 (CTGF/CCN2), which can promote osteoclast formation via upregulation of dendritic cell-specific transmembrane protein (DC-STAMP). On the other hand, overexpression of miR-26a inhibitor enhanced RANKL-induced osteoclast formation and function as well as CTGF expression. In addition, the inhibitory effect of miR-26a on osteoclast formation and function was prevented by treatment with recombinant CTGF. Collectively, our results suggest that miR-26a modulates osteoclast formation and function through the regulation of CTGF.
Keywords
connective tissue growth factor; osteoclast differentiation; microRNA; RANKL;
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