ArticleJournal of gastroenterology2008
Downregulation of CPI-17 contributes to dysfunctional motility in chronic intestinal inflammation model mice and ulcerative colitis patients.
Article in Journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 32 citations in OpenAlex.
- Review
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- Intestinal muscularis in health and disease.Communications biology · 2026Review
- Systemic pathways linking subcutaneous therapies to gastrointestinal adverse effects: A Narrative review of mechanisms and mitigation strategies.Indian journal of pharmacology · 2026Review
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- Human bocavirus 1 viremia-associated pediatric sepsis with a triphasic urinary course: a case report.Translational pediatrics · 2026Article
- Diagnosing Ulcerative Colitis: Should We Go Beyond the Surface?Journal of clinical medicine · 2025Review
- The interplay between alterations in esophageal microbiota associated with Th17 immune response and impaired LC20 phosphorylation in achalasia.Journal of gastroenterology · 2024Article
- Non-invasive neuromodulation: an emerging intervention for visceral pain in gastrointestinal disorders.Bioelectronic medicine · 2023Review
- Altered functional responses by PAR1 agonist in murine dextran sodium sulphate-treated colon.Scientific reports · 2022Article
- Current understanding of Hirschsprung-associated enterocolitis: Pathogenesis, diagnosis and treatment.Seminars in pediatric surgery · 2022Review
- Age-associated changes in microglia and astrocytes ameliorate blood-brain barrier dysfunction.Molecular therapy. Nucleic acids · 2021Article
- Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Transcriptional Suppression of CPI-17 Gene Expression in Vascular Smooth Muscle Cells by Tumor Necrosis Factor, Krüppel-Like Factor 4, and Sp1 Is Associated with Lipopolysaccharide-Induced Vascular Hypocontractility, Hypotension, and Mortality.Molecular and cellular biology · 2019Article
- Network-Based Selection of Candidate Markers and Assays to Assess the Impact of Oral Immune Interventions on Gut Functions.Frontiers in immunology · 2019Article
- Induction of myosin light chain kinase and CPI-17 by TGF-β accelerates contractile activity in intestinal epithelial cells.The Journal of veterinary medical science · 2018Article
- The effect of sphingosine-1-phosphate on colonic smooth muscle contractility: Modulation by TNBS-induced colitis.PloS one · 2017Article
- Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles.Journal of neurogastroenterology and motility · 2016Review
- An integrative view of microbiome-host interactions in inflammatory bowel diseases.Cell host & microbe · 2015Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic intestinal inflammation is frequently accompanied by motility disorders. We previously reported that proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin (IL)-1beta downregulate CPI-17, an endogenous inhibitor of serine/threonine protein phosphatase in smooth-muscle cells, which results in the inhibition of myosin light chain phosphorylation and contractility. However, its clinical relevance has not been clarified.
methodsThe present study examined the changes in CPI-17 expression in chronic intestinal inflammation using smooth-muscle tissues from IL-10 knockout mice and from patients with ulcerative colitis (UC).
resultsThe IL-10 knockout mice developed spontaneous and chronic colitis accompanied by immune cell infiltration, submucosal fibrosis, and thickening of the muscularis externa. The expression of alpha-smooth muscle actin protein in the smooth-muscle layer did not change, whereas that of CPI-17 protein was decreased by about 40% compared with healthy wild-type controls. Consistent with this observation, smooth-muscle contractile force and myosin light chain phosphorylation induced by a muscarinic agonist were reduced in the knockout mice. Moreover, we observed that CPI-17 protein expression was decreased in smooth-muscle tissues from patients with UC compared with controls.
conclusionsCPI-17 downregulation might contribute to the decreased motor function in chronic inflammatory bowel diseases.
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