Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation

Chung Hyeon Choe; In Sun Park; Jisang Park; Kang Yeol Yu; Hyonseok Jang; Ju Kim; Yong Suk Jang

doi:10.1016/j.febslet.2015.02.018

Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation

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

Research output: Contribution to journal › Article › peer-review

13 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 language	English
Article number	37040
Pages (from-to)	836-841
Number of pages	6
Journal	FEBS Letters
Volume	589
Issue number	7
DOIs	https://doi.org/10.1016/j.febslet.2015.02.018
Publication status	Published - 2015 Mar 24
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by Basic Science Research Program through the National Research Foundation of Korea ( NRF ) funded by Korean Ministry of Science, ICT & Future Planning ( 2011-0022168 ) and R&D Program funded by the Provincial Government of Jeollabuk-do . Mr. J. Park was supported by the BK21 Plus program in the Department of Bioactive Material Sciences.

Publisher Copyright:
© 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Keywords

Osteoclastogenesis
RANK ligand
Tartrate-resistant acid phosphatase
Transmembrane protein 173

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2015.02.018

Cite this

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title = "Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation",

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.",

keywords = "Osteoclastogenesis, RANK ligand, Tartrate-resistant acid phosphatase, Transmembrane protein 173",

author = "Choe, {Chung Hyeon} and Park, {In Sun} and Jisang Park and Yu, {Kang Yeol} and Hyonseok Jang and Ju Kim and Jang, {Yong Suk}",

note = "Funding Information: This study was supported by Basic Science Research Program through the National Research Foundation of Korea ( NRF ) funded by Korean Ministry of Science, ICT & Future Planning ( 2011-0022168 ) and R&D Program funded by the Provincial Government of Jeollabuk-do . Mr. J. Park was supported by the BK21 Plus program in the Department of Bioactive Material Sciences. Publisher Copyright: {\textcopyright} 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.",

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doi = "10.1016/j.febslet.2015.02.018",

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AU - Choe, Chung Hyeon

AU - Park, In Sun

AU - Park, Jisang

AU - Yu, Kang Yeol

AU - Jang, Hyonseok

AU - Kim, Ju

AU - Jang, Yong Suk

N1 - Funding Information: This study was supported by Basic Science Research Program through the National Research Foundation of Korea ( NRF ) funded by Korean Ministry of Science, ICT & Future Planning ( 2011-0022168 ) and R&D Program funded by the Provincial Government of Jeollabuk-do . Mr. J. Park was supported by the BK21 Plus program in the Department of Bioactive Material Sciences. Publisher Copyright: © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

PY - 2015/3/24

Y1 - 2015/3/24

N2 - 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.

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.

KW - Osteoclastogenesis

KW - RANK ligand

KW - Tartrate-resistant acid phosphatase

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Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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