Vasoactive Intestinal Peptide

Fahrenkrug, Jan

doi:10.1002/cphy.cp060225

Cited by 7 publications

(5 citation statements)

References 244 publications

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“…VIP is normally expressed in all layers of the gastrointestinal system [9]. In rat and guinea pig, a large proportion of all cell bodies in the submucosal plexus of the ileum and colon are VIP immunoreactive.…”

Section: Discussionmentioning

confidence: 99%

“…It belongs to a family of neuropeptides that include PACAP (pituitary adenylate cyclase-activating polypeptide), which is structurally 70% identical to VIP. All major layers of each segment of the gastrointestinal tract contain VIP-immunoreactive fibers [8,9]. The effects of this neuropeptide in the gastrointestinal system have been extensively studied, and include alterations of motility in the bowel and gallbladder, stimulation of gastric acid and intestinal secretion, hormone/enzyme release from the exocrine and endocrine pancreas, and altered proliferation and survival of tumoral cells (e.g.…”

Section: Introductionmentioning

confidence: 99%

“…The effects of this neuropeptide in the gastrointestinal system have been extensively studied, and include alterations of motility in the bowel and gallbladder, stimulation of gastric acid and intestinal secretion, hormone/enzyme release from the exocrine and endocrine pancreas, and altered proliferation and survival of tumoral cells (e.g. human adenocarcinoma colonic cells) [9,10]. VIP exerts these actions by way of two receptors that belong to the G protein-coupled receptor family, VPAC1 and VPAC2, and which also bind PACAP with high affinity [11].…”

Section: Introductionmentioning

confidence: 99%

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Vasoactive Intestinal Peptide-Deficient Mice Exhibit Reduced Pathology in Trinitrobenzene Sulfonic Acid-Induced Colitis

Cheung-Lau¹,

Coûté-Monvoisin²,

Waschek³

2014

Neuroimmunomodulation

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Objectives: Vasoactive intestinal peptide (VIP) is an immunomodulatory neuropeptide with therapeutic properties in multiple murine models of inflammatory disease including the trinitrobenzene-sulfonic acid (TNBS)-colitis model of Crohn's disease. Understanding the spectrum of biological actions of endogenously produced VIP may help us dissect the complex and multifactorial pathogenesis of such inflammatory diseases. Our goal was to determine the contribution of endogenously produced VIP to TNBS-colitis by using VIP knockout (KO) mice. Methods: TNBS was intracolonically administered to wild-type (WT) and VIP KO mice, and weight loss and colitis were assessed over time. Colon histopathological changes and myeloperoxidase activities were analyzed and the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in colon and serum quantified. The proliferative response in vitro of splenocytes from TNBS WT and VIP KO administered mice to anti-CD3 and anti-CD28 was determined. Results: VIP KO mice did not exhibit the predicted exacerbated response to TNBS. Instead, they developed a milder clinical profile than WT mice, with lower TNF-α and IL-6 levels. Such potential defects seem selective, because other parameters such as the histopathological scores and the cytokine levels in the colon did not differ between the two strains of mice. Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. Conclusion: Chronic loss of VIP in mice leads to a disruption of certain but not all immunological compartments, corroborating recent findings that VIP KO mice exhibit reduced mortality in the lipopolysaccharide-induced endotoxemia model and attenuated clinical development of experimental autoimmune encephalomyelitis while developing robust T-cell responses.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vasoactive Intestinal Peptide-Deficient Mice Exhibit Reduced Pathology in Trinitrobenzene Sulfonic Acid-Induced Colitis

Cheung-Lau¹,

Coûté-Monvoisin²,

Waschek³

2014

Neuroimmunomodulation

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“…VIP is a 28 amino acid polypeptide that has a wide spectrum of biological effects in vertebrates, including the digestive tract, heart, brain, endocrine glands, and the immune system (10). VIP is a member of a superfamily of related peptides, which includes PACAP, PHI, and GHRH (19).…”

Section: Discussionmentioning

confidence: 99%

“…VASOACTIVE INTESTINAL PEPTIDE (VIP) is a neurotransmitter and neuroendocrine hormone first isolated from porcine intestine (29). In numerous mammalian species, this peptide causes smooth muscle relaxation, vasodilation, exocrine secretion in the pancreas, and electrolyte and water secretion by intestinal epithelia (10,18,28). VIP is a member of a large family of structurally related peptides that bind to Class II G proteincoupled receptors, including secretin, pituitary adenylate cyclase activating polypeptide (PACAP), peptide histidine isoleucine (PHI), and growth hormone-releasing hormone (GHRH) (19).…”

mentioning

confidence: 99%

Shark rectal gland vasoactive intestinal peptide receptor: cloning, functional expression, and regulation of CFTR chloride channels

Bewley¹,

Pena²,

Plesch³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Vasoactive intestinal peptide (VIP) is a secretagogue that mediates chloride secretion in intestinal epithelia. We determined the relative potency of VIP and related peptides in the rectal gland of the elasmobranch dogfish shark and cloned and expressed the VIP receptor (sVIP-R) from this species. In the perfused rectal gland, VIP (5 nM) stimulated chloride secretion from 250 +/- 66 to 2,604 +/- 286 microeq x h(-1) x g(-1); the relative potency of peptide agonists was VIP > PHI = GHRH > PACAP > secretin, where PHI is peptide histidine isoleucine amide, GHRH is growth hormone-releasing hormone, and PACAP is pituitary adenylate cylase activating peptide. The cloned sVIP-R from shark rectal gland (SRG) is only 61% identical to the human VIP-R1. It maintains a long, extracellular NH2 terminus with seven cysteine residues, and has three N-glycosylation sites and eight other residues implicated in VIP binding. Two amino acids considered important for peptide binding in mammals are not present in the shark orthologue. When sVIP-R and the CFTR chloride channel were coexpressed in Xenopus oocytes, VIP increased chloride conductance from 11.3 +/- 2 to 127 +/- 34 microS. The agonist affinity for activating chloride conductance by the cloned receptor was VIP > GHRH = PHI > PACAP > secretin, a profile mirroring that in the perfused gland. The receptor differs from previously cloned VIP-Rs in having a low affinity for PACAP. Expression of both sVIP-R and CFTR mRNA was detected by quantitative PCR in shark rectal gland, intestine, and brain. These studies characterize a unique G protein-coupled receptor from the shark rectal gland that is the oldest cloned VIP-R.

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