ArticleInflammatory bowel diseases2010
Ablation of gly96/immediate early gene-X1 (gly96/iex-1) aggravates DSS-induced colitis in mice: role for gly96/iex-1 in the regulation of NF-kappaB.
Article in Inflammatory bowel diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
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- Fermented Alfalfa Meal Instead of "Grain-Type" Feedstuffs in the Diet Improves Intestinal Health Related Indexes in Weaned Pigs.Frontiers in microbiology · 2021Article
- The Capacity of the Ovarian Cancer Tumor Microenvironment to Integrate Inflammation Signaling Conveys a Shorter Disease-free Interval.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Leukemia Inhibitory Factor Inhibits Plasmacytoid Dendritic Cell Function and Development.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Dysregulated IER3 Expression is Associated with Enhanced Apoptosis in Titin-Based Dilated Cardiomyopathy.International journal of molecular sciences · 2017Article
- The RNA-binding protein TTP is a global post-transcriptional regulator of feedback control in inflammation.Nucleic acids research · 2016Article
- IF-combined smRNA FISH reveals interaction of MCPIP1 protein with IER3 mRNA.Biology open · 2016Article
- Wogonin suppresses inflammatory response and maintains intestinal barrier function via TLR4-MyD88-TAK1-mediated NF-κB pathway in vitro.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- Mitochondrial anti-oxidant protects IEX-1 deficient mice from organ damage during endotoxemia.International immunopharmacology · 2014Article
- Translational regulation of specific mRNAs controls feedback inhibition and survival during macrophage activation.PLoS genetics · 2014Article
- Modulation of nuclear factor E2-related factor-2 (Nrf2) activation by the stress response gene immediate early response-3 (IER3) in colonic epithelial cells: a novel mechanism of cellular adaption to inflammatory stress.The Journal of biological chemistry · 2014Article
- Baicalin down regulates the expression of TLR4 and NFkB-p65 in colon tissue in mice with colitis induced by dextran sulfate sodium.International journal of clinical and experimental medicine · 2014Article
- Carboxypeptidase E modulates intestinal immune homeostasis and protects against experimental colitis in mice.PloS one · 2014Article
- Protein kinase C iota in the intestinal epithelium protects against dextran sodium sulfate-induced colitis.Inflammatory bowel diseases · 2011Article
- Impaired immune tolerance to Porphyromonas gingivalis lipopolysaccharide promotes neutrophil migration and decreased apoptosis.Infection and immunity · 2010Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundInflammatory bowel diseases (IBDs) result from environmental and genetic factors and are characterized by an imbalanced immune response in the gut and deregulated activation of the transcription factor NF-kappaB. Addressing the potential role of gly96/iex-1 in the regulation of NF-kappaB in IBD, we used the dextran sodium sulfate (DSS) colitis model in mice in which the gly96/iex-1 gene had been deleted.
methodsC57BL/6 mice of gly96/iex-1(-/-) or gly96/iex-1(+/+) genotype were treated continuously with 4% DSS (5 days) and repeatedly with 2% DSS (28 days) for inducing acute and chronic colitis, respectively. In addition to clinical and histological exploration, colon organ culture and bone marrow-derived cells (BMCs) were analyzed for chemo/cytokine expression and NF-kappaB activation.
resultsCompared to wildtype littermates, gly96/iex-1(-/-) mice exhibited an aggravated phenotype of both acute and chronic colitis, along with a greater loss of body weight and colon length. Colonic endoscopy revealed a higher degree of hyperemia, edema, and bleeding in gly96/iex-1(-/-) mice, and immunohistochemistry detected massive mucosal infiltration of leukocytes and marked histological changes. The expression of proinflammatory chemo- and cytokines was higher in the colon of DSS-treated gly96/iex-1(-/-) mice, and the NF-kappaB activation was enhanced particularly in the distal colon. In cultured BMCs from gly96/iex-1(-/-) mice, Pam(3)Cys(4) treatment induced expression of proinflammatory mediators to a higher degree than in gly96/iex-1(+/+) BMCs, along with greater NF-kappaB activation.
conclusionsBased on the observation that genetic ablation of gly96/iex-1 triggers intestinal inflammation in mice, we demonstrate for the first time that gly96/iex-1 exerts strong antiinflammatory activity via its NF-kappaB-counterregulatory effect.
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