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KMID : 0578320150380010075
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Molecules and Cells
2015 Volume.38 No. 1 p.75 ~ p.80
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MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation
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Kim Kab-Sun
Kim Jung-Ha
Kim In-Young
Lee Jong-Won
Seong Se-Mun
Park Yong-Wook
Kim Nack-Sung
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Abstract
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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 up-regulated 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 up-regulation 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.
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KEYWORD
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connective tissue growth factor, osteoclast differentiation, microRNA, RANKL
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