Disease relevance of Vip

• Vasoactive intestinal polypeptide suppressed experimental autoimmune encephalomyelitis by inhibiting T helper 1 responses [1].
• Immunohistochemical studies of leucine-enkephalin, somatostatin, vasoactive intestinal polypeptide and neurotensin were carried out in dissociated cell co-cultures of embryonic mouse spinal cord and dorsal root ganglion, using the peroxidase-antiperoxidase technique [2].
• Thus there are transitory changes in the innervation of the mouse bladder by vasoactive intestinal polypeptide-containing and cholinergic nerve fibres after exposure to a central demyelinating agent which may reflect changes in bladder dysfunction seen in multiple sclerosis patients [3].
• We also observed a decrease of NPY and vasoactive intestinal polypeptide levels in the hypothalamus of lupus prone mice and these changes may be related to the disregulation of the hypothalamus-pituitary-adrenal axis observed in lupus prone mice [4].
• Gp96 is a receptor for a novel Listeria monocytogenes virulence factor, Vip, a surface protein [5].

Psychiatry related information on Vip

• CONCLUSION: Psychological stress inhibits the small intestinal transit, probably by down-regulating CCK and up-regulating VIP expression in small intestine [6].

High impact information on Vip

• We report here that vasoactive intestinal polypeptide and noradrenaline act synergistically to stimulate the formation of cyclic AMP and that this synergistic interaction is antagonized by the specific alpha-adrenergic antagonist phentolamine [7].
• We have examined this last possibility in the cerebral cortex, an area of the CNS where the two neurotransmitters vasoactive intestinal polypeptide and noradrenaline are contained in separate neuronal systems and where they both stimulate the formation of cyclic AMP [7].
• Critically, daily application of a VPAC(2) agonist restored rhythmicity and synchrony to VIP(-/-) SCN neurons, but not to Vipr2(-/-) neurons [8].
• The concentrations of two intestinally active secretogogues, plasma serotonin and vasoactive intestinal polypeptide, were also measured [9].
• Expression of vasoactive intestinal polypeptide and amylase in a human parotid gland adenocarcinoma cell line in culture [10].

Chemical compound and disease context of Vip

• Vasoactive intestinal polypeptide stimulates cyclic AMP production in mouse N1E-115 neuroblastoma cells: modulation by a protein kinase C activator and ionomycin [11].
• Synthesis and release of vasoactive intestinal polypeptide (VIP) by mouse neuroblastoma cells: modulation by cyclic nucleotides and ascorbic acid [12].
• Met-enkephalin immunoreactivity was localized in multipolar medium sized neurons while VIP immunoreactivity was visualized both in neurons with extensively branched processes and in bipolar cells some of which appeared to be dorsal root ganglion cells [13].
• VIP KO mice showed: (a) airway hyperresponsiveness to the cholinergic agonist methacholine, as well as peribronchial and perivascular inflammation; (b) a greater susceptibility to death from endotoxemia; and (c) evidence suggestive of pulmonary hypertension [14].

Biological context of Vip

• These original data demonstrate that functional GPCRs for VIP and PACAP are present on ES cells and that these neuropeptides may induce their differentiation into a neuronal phenotype [15].
• A similar effect by VIP was also observed in cell migration to fibronectin [16].
• Effects of psychological stress on small intestinal motility and expression of cholecystokinin and vasoactive intestinal polypeptide in plasma and small intestine in mice [6].
• These results strongly suggest that PACAP stimulates cAMP production via an independent binding site from VIP in osteoblast-like MC3T3-E1 cells and that PACAP has no effect on the activation of protein kinase C nor the intracellular Ca2+ mobilization in these cells [17].
• Vasoactive intestinal polypeptide induces glycogenolysis in mouse cortical slices: a possible regulatory mechanism for the local control of energy metabolism [18].

Anatomical context of Vip

• In smooth muscle strips from wild-type and knockout mice, the concentration-dependent relaxation by VIP (10(-9) to 3 x 10(-7) M) was not influenced by L-NA or 1400W [19].
• Relaxation by vasoactive intestinal polypeptide in the gastric fundus of nitric oxide synthase-deficient mice [19].
• VIP and PACAP induce selective neuronal differentiation of mouse embryonic stem cells [15].
• VIP and PACAP potently increased the proportion of EB-derived cells expressing specifically a neuronal phenotype shown by immunocytochemistry and neurite outgrowth without altering glial cell number [15].
• We failed to detect the expression of VIP mRNA in T lymphocytes, from either intestine or spleen [20].

Associations of Vip with chemical compounds

• The influence of NOS inhibitors on the relaxant effect of VIP was determined in isolated smooth muscle cells and smooth muscle strips of wild-type and knockout mice [19].
• The suppressed ability of the tumor cell motility by VIP (10(-6) M) was practically recovered by co-treatment with 2',5'-dideoxyadenosine, an adenylate cyclase inhibitor [16].
• Either PACAP or VIP had little effect on the formation of inositol phosphates and Ca2+ influx in these cells [17].
• Octreotide also reduced synergistic amylase secretion by secretin or VIP in combination with calcium ionophore A23187 [21].
• Octreotide (100 nM) had no inhibitory effects on amylase secretion stimulated by secretin or vasoactive intestinal polypeptide (VIP), while reducing the increase of cyclic adenosine 3',5'-monophosphate (cAMP) [21].

Physical interactions of Vip

• The presence of vasoactive intestinal polypeptide (VIP) receptors coupled to an adenylate cyclase was demonstrated on membranes of neurons or glial cells grown in primary cultures originating from the cerebral cortex, striatum, and mesencephalon of mouse embryos [22].

Regulatory relationships of Vip

• Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are neuropeptides expressed in early development which affect neuronal precursor proliferation and neuronal differentiation [15].
• Gastrin-releasing peptide promotes suprachiasmatic nuclei cellular rhythmicity in the absence of vasoactive intestinal polypeptide-VPAC2 receptor signaling [23].
• [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP, and antagonist for the VIP receptor which markedly inhibited the VIP-induced cAMP accumulation, had little effect on the PACAP-induced cAMP accumulation [17].
• Moreover, VIP-evoked responses from control SCN neurons were attenuated by the selective VPAC2 receptor antagonist PG 99-465 [24].
• It has previously been described that vasoactive intestinal polypeptide (VIP) is a potent potentiator of this cholinergically induced glucagon secretion [25].

Other interactions of Vip

• In cells isolated from iNOS knockout mice, VIP still induced full relaxation but it was not influenced by L-NA or 1400W [19].
• Mouse ES cells were allowed to aggregate in embryoid bodies (EBs) in the presence or not of VIP and PACAP for 1 week [15].
• In addition, VIPR1 mRNA was detected in splenic T lymphocytes, but no signal was obtained for VIPR2 mRNA, even after stimulation of the cells with anti-CD3(epsilon)-chain mAb, phorbol 12-myristate 13-acetate (PMA) and/or VIP [20].
• CCK and VIP levels in plasma and small intestine in mice were measured by radioimmunoassay (RIA) [6].
• VIP and CGRP had small relaxant effects [26].

Analytical, diagnostic and therapeutic context of Vip

• In-vitro treatment with VIP resulted in a tendency towards an increased size of the VIP immunoreactive T cell population and significantly enhanced the average immunofluorescence intensity of the surface labelling [20].
• VIP levels in small intestine were significantly higher in psychological stress mice than those in the control group (8.45+/-1.09 microg/g vs 7.03+/-2.36 microg/g, P<0.01), while there was no significant difference in plasma VIP levels between the two groups [6].
• The results are consistent with the idea that the constriction of the aganglionic segment of colon develops as a consequence of lack of intrinsic inhibitory neurons, possibly those containing vasoactive intestinal polypeptide [27].
• Vasoactive intestinal polypeptide induces analgesia and impairs the antinociceptive effect of morphine in mice [28].
• A monoclonal antibody to vasoactive intestinal polypeptide (VIP) was reduced and alkylated and its light and heavy chains were purified by denaturing gel filtration [29].

References