Retinoblastoma protein-interacting zinc finger 1 (RIZ1) participates in RANKL-induced osteoclast formation via regulation of NFATc1 expression

Abu Shadat Mohammod Noman; Naoki Koide; Imtiaz Iftakhar-E-Khuda; Jargalsaikhan Dagvadorj; Gantsetseg Tumurkhuu; Yoshikazu Naiki; Takayuki Komatsu; Tomoaki Yoshida; Takashi Yokochi

doi:10.1016/j.imlet.2010.04.006

Retinoblastoma protein-interacting zinc finger 1 (RIZ1) participates in RANKL-induced osteoclast formation via regulation of NFATc1 expression

Immunol Lett. 2010 Jul 8;131(2):166-9. doi: 10.1016/j.imlet.2010.04.006. Epub 2010 Apr 24.

Authors

Abu Shadat Mohammod Noman¹, Naoki Koide, Imtiaz Iftakhar-E-Khuda, Jargalsaikhan Dagvadorj, Gantsetseg Tumurkhuu, Yoshikazu Naiki, Takayuki Komatsu, Tomoaki Yoshida, Takashi Yokochi

Affiliation

¹ Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.

PMID: 20417662
DOI: 10.1016/j.imlet.2010.04.006

Abstract

The role of retinoblastoma protein-interacting zinc finger 1 (RIZ1) in receptor activator of NF-kappaB ligand (RANKL)-induced osteoclast formation was examined in mouse RAW 264.7 macrophage-like cells. The expression of RIZ1 was significantly augmented by RANKL-treated cells. Silencing of RIZ1 with the siRNA significantly reduced the appearance of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells as osteoclasts in RANKL-treated cells. The expression of nuclear factor of activated T cell 1 (NFATc1) as the terminal transcription factor of osteoclast formation was prevented by RIZ1 siRNA. It was suggested that that RIZ1 might participate in RANKL-induced osteoclast formation through the regulation of NFATc1 expression.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Acid Phosphatase / biosynthesis
Animals
Antigens, Differentiation / biosynthesis
Bone Resorption
Cell Line
Gene Expression Regulation
Histone-Lysine N-Methyltransferase / genetics
Histone-Lysine N-Methyltransferase / immunology
Histone-Lysine N-Methyltransferase / metabolism*
Isoenzymes / biosynthesis
Macrophages / immunology
Macrophages / metabolism*
Macrophages / pathology
Mice
NFATC Transcription Factors / biosynthesis*
NFATC Transcription Factors / genetics
Neoplasms / metabolism*
Neoplasms / pathology
Neoplasms / physiopathology
Osteoclasts / immunology
Osteoclasts / metabolism*
Osteoclasts / pathology
RANK Ligand / metabolism
RNA, Small Interfering / genetics
Signal Transduction / genetics
Signal Transduction / immunology
Tartrate-Resistant Acid Phosphatase
Transcription Factors / genetics
Transcription Factors / immunology
Transcription Factors / metabolism*

Substances

Antigens, Differentiation
Isoenzymes
NFATC Transcription Factors
RANK Ligand
RNA, Small Interfering
Tnfsf11 protein, mouse
Transcription Factors
Histone-Lysine N-Methyltransferase
Prdm2 protein, mouse
Acid Phosphatase
Acp5 protein, mouse
Tartrate-Resistant Acid Phosphatase