ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Homeostatic and therapeutic roles of VIP in smooth muscle function: myo-neuroimmune interactions.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- TNBS colitis induces architectural changes and alpha-synuclein overexpression in mouse distal colon: A morphological study.Cell and tissue research · 2025Article
- The Role of Inflammatory Mediators in the Development of Gastrointestinal Motility Disorders.International journal of molecular sciences · 2022Review
- Vasoactive Intestinal Polypeptide (VIP) in the Intestinal Mucosal Nerve Fibers in Dogs with Inflammatory Bowel Disease.Animals : an open access journal from MDPI · 2020Article
- Recommendations for evaluation of bladder and bowel function in pre-clinical spinal cord injury research.The journal of spinal cord medicine · 2020Review
- Neurochemistry of Enteric Neurons Following Prolonged Indomethacin Administration in the Porcine Duodenum.Frontiers in pharmacology · 2020Article
- Tumor necrosis factor alpha derived from classically activated "M1" macrophages reduces interstitial cell of Cajal numbers.Neurogastroenterology and motility · 2017Article
- Mechanisms of smooth muscle responses to inflammation.Neurogastroenterology and motility · 2012Review
- Ion channel remodeling in gastrointestinal inflammation.Neurogastroenterology and motility · 2010Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We tested the hypothesis that spontaneous release of vasoactive intestinal peptide (VIP) from enteric neurons maintains homeostasis in smooth muscle function in mild inflammatory insults and that infusion of exogenous VIP has therapeutic effects on colonic smooth muscle dysfunction in inflammation. In vitro experiments were performed on human colonic circular smooth muscle tissues and in vivo on rats. The incubation of human colonic circular smooth muscle strips with TNF-alpha suppressed their contractile response to ACh and the expression of the pore-forming alpha(1C) subunit of Ca(v)1.2 channels. VIP reversed both effects by blocking the translocation of NF-kappaB to the nucleus and its binding to the kappaB recognition sites on halpha(1C)1b promoter. The translocation of NF-kappaB was inhibited by blocking the degradation of IkappaBbeta. Induction of inflammation by a subthreshold dose of 17 mg/kg trinitrobenzene sulfonic acid (TNBS) in rats moderately decreased muscularis externa concentration of VIP, and it had little effect on the contractile response of circular smooth muscle strips to ACh. The blockade of VIP and pituitary adenylate cyclase-activating peptide receptors 1/2 during mild inflammatory insult significantly worsened the suppression of contractility and the inflammatory response. The induction of more severe inflammation by 68 mg/kg TNBS induced marked suppression of colonic circular muscle contractility and decrease in serum VIP. Exogenous infusion of VIP by an osmotic pump reversed these effects. We conclude that the spontaneous release of VIP from the enteric motor neurons maintains homeostasis in smooth muscle function in mild inflammation by blocking the activation of NF-kappaB. The infusion of exogenous VIP mitigates colonic inflammatory response and smooth muscle dysfunction.
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