ID 110882
Author
Sasaki, Hideyuki Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
Yamamoto, Hironori Departments of Clinical Nutrition, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN Search Researchers
Tominaga, Kumiko Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
Masuda, Kiyoshi Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN Search Researchers
Kawai, Tomoko Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
Teshima-Kondo, Shigetada Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN Search Researchers
Rokutan, Kazuhito Departments of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
osteoclasts
differentiation
bone resorption
reactive oxygen species
NADPH oxidase
Content Type
Journal Article
Description
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.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
56
Issue
1-2
Start Page
33
End Page
41
Sort Key
33
Published Date
2009-02
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Medical Sciences