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)
  • Received : 2014.09.02
  • Accepted : 2014.10.17
  • Published : 2015.01.31


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.


connective tissue growth factor;osteoclast differentiation;microRNA;RANKL


Supported by : National Research Foundation of Korea (NRF)


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