Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation

Chung Hyeon Choe, In Sun Park, Jisang Park, Kang Yeol Yu, Hyon Seok Jang, Ju Kim, Yong Suk Jang

Research output: Contribution to journalArticle

5 Citations (Scopus)

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.

Original languageEnglish
Article number37040
Pages (from-to)836-841
Number of pages6
JournalFEBS Letters
Volume589
Issue number7
DOIs
Publication statusPublished - 2015 Mar 24

Fingerprint

Osteoclasts
Proteins
Chemical activation
Cathepsin K
NFATC Transcription Factors
Growth Inhibitors
Macrophages
Matrix Metalloproteinase 9
Bone Resorption
Acid Phosphatase
Major Histocompatibility Complex
Osteogenesis
Bone
Transcription Factors
Genes
Feedback
Controllers

Keywords

  • Osteoclastogenesis
  • RANK ligand
  • Tartrate-resistant acid phosphatase
  • Transmembrane protein 173

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Choe, C. H., Park, I. S., Park, J., Yu, K. Y., Jang, H. S., Kim, J., & Jang, Y. S. (2015). Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation. FEBS Letters, 589(7), 836-841. [37040]. https://doi.org/10.1016/j.febslet.2015.02.018

Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation. / Choe, Chung Hyeon; Park, In Sun; Park, Jisang; Yu, Kang Yeol; Jang, Hyon Seok; Kim, Ju; Jang, Yong Suk.

In: FEBS Letters, Vol. 589, No. 7, 37040, 24.03.2015, p. 836-841.

Research output: Contribution to journalArticle

Choe, CH, Park, IS, Park, J, Yu, KY, Jang, HS, Kim, J & Jang, YS 2015, 'Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation', FEBS Letters, vol. 589, no. 7, 37040, pp. 836-841. https://doi.org/10.1016/j.febslet.2015.02.018
Choe, Chung Hyeon ; Park, In Sun ; Park, Jisang ; Yu, Kang Yeol ; Jang, Hyon Seok ; Kim, Ju ; Jang, Yong Suk. / Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation. In: FEBS Letters. 2015 ; Vol. 589, No. 7. pp. 836-841.
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AB - 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.

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