ArticlePloS one2014
Combined NADPH oxidase 1 and interleukin 10 deficiency induces chronic endoplasmic reticulum stress and causes ulcerative colitis-like disease in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Ameliorative Effect of Banana Lectin in TNBS-Induced Colitis in C57BL/6 Mice Relies on the Promotion of Antioxidative Mechanisms in the Colon.Biomolecules · 2025Article
- The SYSCID map: a graphical and computational resource of molecular mechanisms across rheumatoid arthritis, systemic lupus erythematosus and inflammatory bowel disease.Frontiers in immunology · 2023Article
- The Heterochromatin protein 1 is a regulator in RNA splicing precision deficient in ulcerative colitis.Nature communications · 2022Article
- Carnosol Maintains Intestinal Barrier Function and Mucosal Immune Homeostasis in DSS-Induced Colitis.Frontiers in nutrition · 2022Article
- NOX1 Regulates Collective and Planktonic Cell Migration: Insights From Patients With Pediatric-Onset IBD and NOX1 Deficiency.Inflammatory bowel diseases · 2020Article
- Interleukin-4 Receptor α Subunit Deficiency Alleviates Murine Intestinal Inflammation In Vivo Through the Enhancement of Intestinal Mucosal Barrier Function.Frontiers in pharmacology · 2020Article
- NADPH oxidases and ROS signaling in the gastrointestinal tract.Mucosal immunology · 2018Review
- NOX1 loss-of-function genetic variants in patients with inflammatory bowel disease.Mucosal immunology · 2018Article
- NoxO1 Controls Proliferation of Colon Epithelial Cells.Frontiers in immunology · 2018Article
- ROS in gastrointestinal inflammation: Rescue Or Sabotage?British journal of pharmacology · 2017Review
- Therapeutic potential of NADPH oxidase 1/4 inhibitors.British journal of pharmacology · 2017Review
- The ROS-generating oxidase Nox1 is required for epithelial restitution following colitis.Experimental animals · 2016Article
- Article
- Genetic disorders coupled to ROS deficiency.Redox biology · 2015Review
- Knockdown of interleukin-10 induces the redistribution of sigma1-receptor and increases the glutamate-dependent NADPH-oxidase activity in mouse brain neurons.Biological research · 2015Article
- Defects in NADPH Oxidase GenesCellular and molecular gastroenterology and hepatology · 2015Article
- Endoplasmic reticulum stress signaling in mammalian oocytes and embryos: life in balance.International review of cell and molecular biology · 2015Review
- Endoplasmic reticulum stress in intestinal epithelial cell function and inflammatory bowel disease.Gastroenterology research and practice · 2015Review
- Article
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Authors and funding
20 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease affecting the rectum which progressively extents. Its etiology remains unknown and the number of treatments available is limited. Studies of UC patients have identified an unbalanced endoplasmic reticulum (ER) stress in the non-inflamed colonic mucosa. Animal models with impaired ER stress are sensitive to intestinal inflammation, suggesting that an unbalanced ER stress could cause inflammation. However, there are no ER stress-regulating strategies proposed in the management of UC partly because of the lack of relevant preclinical model mimicking the disease. Here we generated the IL10/Nox1dKO mouse model which combines immune dysfunction (IL-10 deficiency) and abnormal epithelium (NADPH oxidase 1 (Nox1) deficiency) and spontaneously develops a UC-like phenotype with similar complications (colorectal cancer) than UC. Our data identified an unanticipated combined role of IL10 and Nox1 in the fine-tuning of ER stress responses in goblet cells. As in humans, the ER stress was unbalanced in mice with decreased eIF2α phosphorylation preceding inflammation. In IL10/Nox1dKO mice, salubrinal preserved eIF2α phosphorylation through inhibition of the regulatory subunit of the protein phosphatase 1 PP1R15A/GADD34 and prevented colitis. Thus, this new experimental model highlighted the central role of epithelial ER stress abnormalities in the development of colitis and defined the defective eIF2α pathway as a key pathophysiological target for UC. Therefore, specific regulators able to restore the defective eIF2α pathway could lead to the molecular remission needed to treat UC.
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