Transmembrane protein 173 inhibits RANKL‐induced osteoclast differentiation. Issue 7 (26th February 2015)

• Record Type: Journal Article
• Authors: Choe, Chung-Hyeon; Park, In Sun; Park, Jisang; Yu, Kang-Yeol; Jang, Hyonseok; Kim, Ju; Jang, Yong-Suk
• Is Part Of: FEBS letters. Volume 589:Issue 7(2015)
• Page Start: 836
• Page End: 841
• Publication Date: 2015-02-26
• Subjects: DMEM -- Dulbecco's Modified Eagle's Media -- FBS -- fetal bovine serum -- HRP -- horseradish peroxidase -- JAK -- Janus kinase -- M-CSF -- macrophage colony-stimulating factor -- MAP -- mitogen-activated protein -- MHC -- major histocompatibility complex -- MMP-9 -- matrix metalloproteinase-9 -- NFATc1 -- nuclear factor of activated T cells cytoplasmic-1 -- OCIF -- osteoclastogenesis inhibitory factor -- OPG -- osteoprotegerin -- p-ERK -- phosphorylated ERK -- RANK -- receptor activator of nuclear factor κB -- RANKL -- RANK ligand -- SERM -- selective estrogen receptor modulator -- STAT -- signal transducer and activator of transcription -- Tmem173 -- transmembrane protein 173 -- TRAP -- tartrate-resistant acid phosphatase -- Osteoclastogenesis -- RANK ligand -- Transmembrane protein 173 -- Tartrate-resistant acid phosphatase; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2015.02.018
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Tmem173 was identified as a growth inhibitor associated with major histocompatibility complex (MHC) class II and a potential stimulator for IFN‐β, an innate immune inducer and a negative feedback controller for RANKL‐induced osteoclast differentiation of monocytic macrophage cells. In this study, we confirmed that transmembrane protein 173 (Tmem173) overexpression inhibited the expression of osteoclast‐specific genes, tartrate‐resistant acid phosphatase (TRAP), cathepsin K, and matrix metalloproteinase‐9 (MMP‐9), as well as bone resorption pit formation in RANKL‐treated RAW 264.7 cells. Activation of osteoclast‐specific transcription factors, c‐Fos and nuclear factor of activated T cells cytoplasmic‐1 (NFATc1), and RANKL‐induced activation of ERK were also down‐regulated by Tmem173 overexpression. Collectively, these results suggest that Tmem173 plays a regulatory role in RANKL–RANK‐mediated signaling in osteoclastogenesis. Abstract : Inhibitory effect of Tmem173 on RANKL‐induced osteoclastogenesis was investigated. Overexpression of Tmem173 inhibited osteoclast‐specific gene expression. Osteoclast‐specific transcription factor activation was also inhibited by Tmem173. OPG, an inhibitor of osteoclastogenesis, activated Tmem173 gene expression. These results suggest a critical role of Tmem173 in RANKL‐induced osteoclastogenesis.