MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation |
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Authors: | Kabsun Kim Jung Ha Kim Inyoung Kim Jongwon Lee Semun Seong Yong-Wook Park Nacksung Kim |
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Affiliation: | Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea;1.Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju 501-757, Korea |
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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 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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Keywords: | connective tissue growth factor osteoclast differentiation microRNA RANKL |
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