Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation

善岡, 克次; Ikeda, Fumiyo; Nishimura, Riko; Matsubara, Takuma; Tanaka, Sakae; Inoue, Jun-ichiro; Reddy, Sakamuri V.; Hata, Kenji; Yamashita, Kenji; Hiraga, Toru; Watanabe, Toshiyuki; Kukita, Toshio; Yoshioka, Katsuji; Rao, Anjana; Yoneda, Toshiyuki

doi:10.1172/JCI200419657

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Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation

https://doi.org/10.24517/00027534

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CA-PR-YOSHIOKA-K-475.pdf (1.0 MB)

Item type

学術雑誌論文 / Journal Article(1)

公開日

2017-10-05

タイトル

Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation

言語

eng

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資源タイプ識別子

http://purl.org/coar/resource_type/c_6501

資源タイプ

journal article

ID登録

10.24517/00027534

ID登録タイプ

JaLC

著者

Ikeda, Fumiyo
Nishimura, Riko

Matsubara, Takuma

Tanaka, Sakae
Inoue, Jun-ichiro

Reddy, Sakamuri V.

Hata, Kenji
Yamashita, Kenji

Hiraga, Toru
Watanabe, Toshiyuki

Kukita, Toshio

Yoshioka, Katsuji

WEKO 142
e-Rad 60200937
金沢大学研究者情報 60200937
研究者番号 60200937

	Yoshioka, Katsuji

Search repository

Rao, Anjana
Yoneda, Toshiyuki

著者別表示

善岡, 克次

提供者所属

内容記述タイプ

Other

内容記述

金沢大学がん研究所がん分子細胞制御

書誌情報

Journal of Clinical Investigation

巻 114, 号 4, p. 475-484, 発行日 2004-08-01

ISSN

収録物識別子タイプ

ISSN

収録物識別子

0021-9738

NCID

収録物識別子タイプ

NCID

収録物識別子

AA00695520

DOI

関連識別子

10.1172/JCI200419657

出版者

American Society for Clinical Investigation

抄録

内容記述タイプ

Abstract

内容記述

Receptor activator of NF-κB ligand (RANKL) plays an essential role in osteoclast formation and bone resorption. Although genetic and biochemical studies indicate that RANKL regulates osteoclast differentiation by activating receptor activator of NF-κB and associated signaling molecules, the molecular mechanisms of RANKL-regulated osteoclast differentiation have not yet been fully established. We investigated the role of the transcription factor c-Jun, which is activated by RANKL, in osteoclastogenesis using transgenic mice expressing dominant-negative c-Jun specifically in the osteoclast lineage. We found that the transgenic mice manifested severe osteopetrosis due to impaired osteoclastogenesis. Blockade of c-Jun signaling also markedly inhibited soluble RANKL-induced osteoclast differentiation in vitro. Overexpression of nuclear factor of activated T cells 1 (NFAT1) (NFATc2/ NFATp) or NFAT2 (NFATc1/NFATc) promoted differentiation of osteoclast precursor cells into tartrate-resistant acid phosphatase-positive (TRAP-positive) multinucleated osteoclast-like cells even in the absence of RANKL. Overexpression of NFAT1 also markedly transactivated the TRAP gene promoter. These osteoclastogenic activities of NFAT were abrogated by overexpression of dominant-negative c-Jun. Importantly, osteoclast differentiation and induction of NFAT2 expression by NFAT1 overexpression or soluble RANKL treatment were profoundly diminished in spleen cells of the transgenic mice. Collectively, these results indicate that c-Jun signaling in cooperation with NFAT is crucial for RANKL-regulated osteoclast differentiation.

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VoR

出版タイプResource

http://purl.org/coar/version/c_970fb48d4fbd8a85

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2023-07-27 11:05:56.921290

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Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation

× Ikeda, Fumiyo

× Nishimura, Riko

× Matsubara, Takuma

× Tanaka, Sakae

× Inoue, Jun-ichiro

× Reddy, Sakamuri V.

× Hata, Kenji

× Yamashita, Kenji

× Hiraga, Toru

× Watanabe, Toshiyuki

× Kukita, Toshio

× Yoshioka, Katsuji

× Rao, Anjana

× Yoneda, Toshiyuki

× 善岡, 克次

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