ID 110882
著者
ササキ, ヒデユキ Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
山本, 浩範 Departments of Clinical Nutrition, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN研究者をさがす
トミナガ, クミコ Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
増田, 清士 Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN研究者をさがす
カワイ, トモコ Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
近藤, 茂忠 Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN研究者をさがす
六反, 一仁 Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
osteoclasts
differentiation
bone resorption
reactive oxygen species
NADPH oxidase
資料タイプ
学術雑誌論文
抄録
Reactive oxygen species (ROS) derived from NADPH oxidase (Nox) homologues have been suggested to regulate osteoclast differentiation. However, no bone abnormalities have been documented in Nox1 deficient, Nox2 deficient, or Nox3 mutant mice. During receptor activator of nuclear factor-κB ligand (RANKL)-stimulated differentiation of a mouse macrophage cell line (RAW264.7) into osteoclasts, mRNA levels of Nox enzymes (Nox1-4) and their adaptor proteins were monitored by real-time reverse transcriptase PCR. RAW264.7 cells constitutively expressed abundant Nox2 mRNA and small amounts of Nox1 and Nox3 transcripts. RANKL markedly attenuated Nox2 mRNA expression in association with reciprocal up-regulation of Nox1 and Nox3 transcripts. Introduction of small interference RNA targeting p67phox or p22phox into RAW264.7 cells effectively downregulated ROS generation and significantly suppressed the RANKL-stimulated differentiation, which was assessed by appearance of tartrate resistant acid phosphatase (TRAP)- positive, multinucleated cells having an ability to form resorption pits on calcium phosphate thin film-coated disks, and by expression of osteoclast marker genes (TRAP, cathepsin K, Atp6i, ClC-7, and NFATc1). Our results suggest that RANKL may stimulate switching between Nox homologues during osteoclast differentiation, and Nox-derived ROS may be crucial for RANKL-induced osteoclast differentiation.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
56
1-2
開始ページ
33
終了ページ
41
並び順
33
発行日
2009-02
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系