Retinoblastoma protein-interacting zinc finger 1, a tumor suppressor, augments lipopolysaccharide-induced proinflammatory cytokine production via enhancing nuclear factor-kappaB activation

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.cellimm.2010.05.007

Retinoblastoma protein-interacting zinc finger 1, a tumor suppressor, augments lipopolysaccharide-induced proinflammatory cytokine production via enhancing nuclear factor-kappaB activation

Cell Immunol. 2010;264(2):114-8. doi: 10.1016/j.cellimm.2010.05.007. Epub 2010 May 27.

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: 20557878
DOI: 10.1016/j.cellimm.2010.05.007

Abstract

The involvement of retinoblastoma protein-interacting zinc finger 1 (RIZ1), a tumor suppressor, in lipopolysaccharide (LPS)-induced inflammatory responses was investigated by using RAW 264.7 macrophage-like cells. LPS significantly augmented the expression of RIZ1 and the augmentation was mediated by the activation of nuclear factor (NF)-kappaB and Akt. The silencing of RIZ1 with the siRNA led to the inactivation of NF-kappaB in response to LPS. Moreover, the RIZ1 silencing caused the down-regulation of p53 activation and a p53 pharmacological inhibitor attenuated the RIZ1 expression. LPS-induced tumor necrosis factor-alpha and interleukin-6 production was prevented by RIZ1 siRNA or a p53 pharmacological inhibitor. Therefore, RIZ1 was suggested to augment LPS-induced NF-kappaB activation in collaboration with p53 and enhance the production of proinflammatory cytokines in response to LPS.

Publication types

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

MeSH terms

Animals
Cell Line
Cloning, Molecular
Histone-Lysine N-Methyltransferase / genetics
Histone-Lysine N-Methyltransferase / immunology
Histone-Lysine N-Methyltransferase / metabolism*
Inflammation
Interleukin-6 / biosynthesis*
Interleukin-6 / genetics
Interleukin-6 / metabolism
Lipopolysaccharides / immunology
Lipopolysaccharides / metabolism
Macrophages / immunology
Macrophages / metabolism*
Macrophages / pathology
Mice
Mutation / genetics
NF-kappa B / genetics
NF-kappa B / metabolism*
RNA, Small Interfering / genetics
Transcription Factors / genetics
Transcription Factors / immunology
Transcription Factors / metabolism*
Transcriptional Activation / genetics
Tumor Necrosis Factor-alpha / biosynthesis*
Tumor Necrosis Factor-alpha / genetics
Tumor Necrosis Factor-alpha / metabolism
Tumor Suppressor Protein p53 / genetics
Tumor Suppressor Protein p53 / metabolism

Substances

Interleukin-6
Lipopolysaccharides
NF-kappa B
RNA, Small Interfering
Transcription Factors
Tumor Necrosis Factor-alpha
Tumor Suppressor Protein p53
Histone-Lysine N-Methyltransferase
Prdm2 protein, mouse