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Interferon‐β‐induced miR‐155 inhibits osteoclast differentiation by targeting SOCS1 and MITF
Author(s) -
Zhang Jun,
Zhao Hongying,
Chen Jinping,
Xia Bing,
Jin Yongming,
Wei Wei,
Shen Jianjian,
Huang Yazeng
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.06.047
Subject(s) - osteoclast , activator (genetics) , microphthalmia associated transcription factor , rankl , signal transduction , rank ligand , microbiology and biotechnology , chemistry , cancer research , cellular differentiation , receptor , biology , transcription factor , biochemistry , gene
IFN‐β is induced via a c‐fos dependent mechanism that is present downstream of the receptor activator of NF‐κB ligand (RANKL)‐RANK signal transduction cascade during osteoclast differentiation. Increased production of IFN‐β in turn inhibits osteoclastogenesis. However, the mechanism by which IFN‐β exerts its suppressive function remains unclear. In the present study, we found that miR‐155, an IFN‐β‐induced miRNA, mediated the suppressive effect of IFN‐β on osteoclast differentiation by targeting SOCS1 and MITF, two essential regulators of osteoclastogenesis. These findings have not only demonstrated that miR‐155 inhibits osteoclast differentiation, but also provided a new therapeutic target for treatment of osteoclast‐mediated diseases.