ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in a model of postinfective IBS.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Systematic review of animal models of post-infectious/post-inflammatory irritable bowel syndrome.Journal of gastroenterology · 2011Pooled it
- Renzhu Ointment Regulates L-Type Voltage-Dependent Calcium Channel in Mice Model of Senna-Induced Diarrhea by Transdermal Administration.Drug design, development and therapy · 2023Article
- Epigenetic Mechanisms in Irritable Bowel Syndrome.Frontiers in psychiatry · 2020Review
- Review
- Ion channels, ion channel receptors, and visceral hypersensitivity in irritable bowel syndrome.Neurogastroenterology and motility · 2016Review
- Enhanced sympathetic nerve activity induced by neonatal colon inflammation induces gastric hypersensitivity and anxiety-like behavior in adult rats.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Inflammation induced by mast cell deficiency rather than the loss of interstitial cells of Cajal causes smooth muscle dysfunction in W/W(v) mice.Frontiers in physiology · 2014Article
- Main ion channels and receptors associated with visceral hypersensitivity in irritable bowel syndrome.Annals of gastroenterology · 2014Review
- Extra-intestinal and long term consequences of Giardia duodenalis infections.World journal of gastroenterology · 2013Review
- Developmental origins of colon smooth muscle dysfunction in IBS-like rats.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Developmental origins of functional dyspepsia-like gastric hypersensitivity in rats.Gastroenterology · 2013Article
- Cell culture retains contractile phenotype but epigenetically modulates cell-signaling proteins of excitation-contraction coupling in colon smooth muscle cells.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Nitric oxide modifies chromatin to suppress ICAM-1 expression during colonic inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Impaired integrity of DNA after recovery from inflammation causes persistent dysfunction of colonic smooth muscle.Gastroenterology · 2011Article
- Hedgehog signaling controls homeostasis of adult intestinal smooth muscle.Developmental biology · 2011Article
- Lessons Learnt from Post-Infectious IBS.Frontiers in physiology · 2011Article
- Chronic stress targets posttranscriptional mechanisms to rapidly upregulate α1C-subunit of Cav1.2b calcium channels in colonic smooth muscle cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Adrenergic stimulation mediates visceral hypersensitivity to colorectal distension following heterotypic chronic stress.Gastroenterology · 2010Article
- Homeostatic and therapeutic roles of VIP in smooth muscle function: myo-neuroimmune interactions.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The cellular mechanisms of motility dysfunction in postinfectious irritable bowel syndrome (PI-IBS) are not known. We used a rat model of neonatal inflammation to test the hypothesis that gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in PI-IBS. Mild/moderate or severe inflammation was induced in neonatal and adult rats. Experiments were performed in tissues obtained at 7 days (short term) and 6-8 wk (long term) after the induction of inflammation. Severe inflammation in neonatal rats induced persistent long-term smooth muscle hyperreactivity to acetylcholine (ACh), whereas that in adult rat caused smooth muscle hyporeactivity that showed partial recovery in the long term. Mild/moderate inflammation had no effect in neonatal rats, but it induced smooth muscle hyporeactivity to ACh in adult rats, which recovered fully in the long term. Smooth muscle hyperreactivity to ACh resulted in accelerated colonic transit and increase in defecation rate, whereas hyporeactivity had opposite effects. Smooth muscle hyperreactivity to ACh was associated with increase in transcription rate of key cell-signaling proteins of the excitation-contraction coupling alpha1C subunit of Cav1.2 (L-type) calcium channels, Galphaq, and 20-kDa myosin light chain (MLC20), whereas hyporeactivity was associated with their suppression. Inflammation in adult rats induced classical inflammatory response, which was absent in neonatal rats. Severe neonatal inflammation enhanced plasma norepinephrine and muscularis propria vasoactive intestinal polypeptide in the long term. We conclude that severe, but not mild/moderate, inflammation in a state of immature or impaired stress and immune response systems alters the transcription rate of key cell-signaling proteins of excitation-contraction coupling in colonic circular smooth muscle cells to enhance their contractility and accelerate colonic transit and defecation rate.
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