C/Ebp Homologous Protein (Chop) is Crucial for the Induction of Caspase-11 and the Pathogenesis of Lipopolysaccharide-induced Inflammation.
From: Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Honjo 1-1-1, Kumamoto 860-8556, Japan.
Journal of immunology (Baltimore, Md. : 1950)
- Publish Date: May 2006
- ISSN: 0022-1767
- Volume: 176
- Issue: 10
- Pages: 6245-53
- Medium: Print
- Language: English
- Citation (JAMA): Endo Motoyoshi, Mori Masataka, Akira Shizuo, et al. C/Ebp Homologous Protein (Chop) is Crucial for the Induction of Caspase-11 and the Pathogenesis of Lipopolysaccharide-induced Inflammation.. J. Immunol. May 2006;176:6245-53
Abstract
C/EBP homologous protein (CHOP)/growth arrest and DNA damage-inducible gene 153 is a C/EBP family transcription factor which is involved in endoplasmic reticulum (ER) stress-mediated apoptosis. To determine whether the ER stress-CHOP pathway is involved in the pathogenesis of the lung inflammation, mice were given LPS intratracheally. Treatment with LPS induced mRNAs for CHOP and BiP. The LPS-induced inflammation in lung, including the IL-1beta activity in bronchoalveolar lavage fluid, was attenuated in the Chop knockout mice. Caspase-11, which is needed for the activation of procaspase-1 and pro-IL-1beta, was induced by LPS treatment in the lung and primary cultured macrophages. The induction of caspase-11 by LPS was suppressed in Chop knockout mice. Caspase-11 was also induced by such ER stress inducers as thapsigargin or tunicamycin. These results show that CHOP plays a crucial role in the pathogenesis of inflammation through the induction of caspase-11.
Mesh Headings (Keywords): Animals, Caspases, Cells, Cultured, Enzyme Induction, Inflammation, Lipopolysaccharides, Lung, Macrophages, Peritoneal, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Transcription Factor CHOP
Check for Full Text / PubMed Unique Identifier (PMID): 16670335
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