ArticleGastroenterology2011
Impaired integrity of DNA after recovery from inflammation causes persistent dysfunction of colonic smooth muscle.
Article in Gastroenterology, 2011. 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, 24 citations in OpenAlex.
- Inflammatory bowel diseases: pathological mechanisms and therapeutic perspectives.Molecular biomedicine · 2026Review
- Ileocolic Intussusception in a Woman: A Case Report and Literature Review.The American journal of case reports · 2021Review
- Fermented Rice Bran Supplementation Prevents the Development of Intestinal Fibrosis Due to DSS-Induced Inflammation in Mice.Nutrients · 2021Article
- Abnormal gut motility in inflammatory bowel disease: an update.Techniques in coloproctology · 2020Review
- Symptoms compatible with functional bowel disorders are common in patients with quiescent ulcerative colitis and influence the quality of life but not the course of the disease.Therapeutic advances in gastroenterology · 2019Article
- Neonatal Colonic Inflammation Epigenetically Aggravates Epithelial Inflammatory Responses to Injury in Adult Life.Cellular and molecular gastroenterology and hepatology · 2018Article
- Isothiocyanate-enriched moringa seed extract alleviates ulcerative colitis symptoms in mice.PloS one · 2017Article
- Genomics of Colorectal Cancer in African Americans.Next generation, sequencing & applications · 2016Article
- Repurposing the NRF2 Activator Dimethyl Fumarate as Therapy Against Synucleinopathy in Parkinson's Disease.Antioxidants & redox signaling · 2016Article
- Red wine polyphenol extract efficiently protects intestinal epithelial cells from inflammationToxicology research · 2016Article
- Identification of novel mutations by exome sequencing in African American colorectal cancer patients.Cancer · 2015Article
- Aging-associated oxidative stress leads to decrease in IAS tone via RhoA/ROCK downregulation.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Gastrointestinal motility disorders in inflammatory bowel diseases.World journal of gastroenterology · 2014Review
- Chemistry meets biology in colitis-associated carcinogenesis.Free radical research · 2013Review
- Nrf2 is not required for epithelial prohibitin-dependent attenuation of experimental colitis.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Mechanisms of smooth muscle responses to inflammation.Neurogastroenterology and motility · 2012Review
- Lessons Learnt from Post-Infectious IBS.Frontiers in physiology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsPatients with inflammatory bowel disease who are in remission and those who developed irritable bowel syndrome after enteric infection continue to have symptoms of diarrhea or constipation in the absence of overt inflammation, indicating motility dysfunction. We investigated whether oxidative stress during inflammation impairs integrity of the promoter of Cacna1c, which encodes the pore-forming α1C subunit of Ca(v)1.2b calcium channels.
methodsWe used long-extension polymerase chain reaction to evaluate DNA integrity in tissues from distal colons of rats; trinitrobenzene sulfonic acid was used to induce inflammation.
resultsThe H2O2 increased in the muscularis externa 1-7 days after inflammation was induced with trinitrobenzene sulfonic acid. The oxidative stress significantly impaired DNA integrity in 2 specific segments of the Cacna1c promoter: -506 to -260 and -2193 to -1542. The impairment peaked at day 3 and recovered partially by day 7 after induction of inflammation; expression of the products of Cacna1c followed a similar time course. Oxidative stress suppressed the expression of nuclear factor-erythroid-2-related factor 2 (Nrf2), an important regulator of anti-oxidant proteins. Intraperitoneal administration of sulforaphane significantly reversed the suppression of Nrf2, oxidative damage in the promoter of Cacna1c, and suppression of Cacna1c on day 7 of inflammation. The inflammation subsided completely by 56 days after inflammation was induced; however, impairment of DNA integrity, expression of Nrf2 and Cacna1c, and smooth muscle reactivity to acetylcholine remained suppressed at this time point.
conclusionsOxidative stress during inflammation impairs the integrity of the promoter of Cacna1c; impairment persists partially after inflammation has subsided. Reduced transcription of Cacna1c contributes to smooth muscle dysfunction in the absence of inflammation.
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Registered trials
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