Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported that pituitary vasoactive intestinal peptide (VIP) mediates through autoparacrine mechanisms insulin-like growth factor-I and TRH-stimulated PRL release. In the present study, we have investigated whether VIP might also be implicated in the PRL increase that follows dopamine (DA) withdrawal. The experiments were carried out in defined medium supplemented or not with T3, as in a previous study we had found that PRL release increases under low T3 culture conditions due to mediation by concomittant stimulus of VIP. Anterior pituitary (AP) cells from adult male rats were incubated for 1 h in the presence of DA (10 microM), a VIP-receptor antagonist (VIP-At) (200 nM), or DA plus VIP-At. Then media were removed and the cells were washed with PBS and reincubated under the same conditions but without the addition of DA. In the first incubation, DA inhibited PRL release by 80%, and VIP release by 20% in both T3-free and T3 medium. In the second period of incubation, PRL and VIP release were increased in AP cells previously exposed to DA. These effects were greater when the cells were cultured in T3-free medium than in T3-medium (225% and 150%, respectively for PRL release; and 155 and 135%, respectively for VIP release). PRL response to DA withdrawal was inhibited by the simultaneous presence of VIP-At. This inhibition was again greater when the cells were incubated in medium supplemented with T2. Thus, the stimulus of DA withdrawal was inhibited by 88% in T2-free medium and by 37% in T3-medium. To investigate whether pituitary VIP messenger RNA (mRNA) expression is under dopaminergic control, AP cells were incubated in the presence or absence of bromocriptine (BC) (10 nM) for 2 and 24 h. After 24 h of incubation, BC decreased mRNA levels of PRL and of the two transcripts which VIP expresses in AP. As with DA, BC also inhibited PRL and VIP release both at 2 and 24 h. These data demonstrate that VIP, at least partially, mediates DA withdrawal-induced PRL release through an autoparacrine action. They also suggest that simultaneous inhibition of pituitary VIP mRNA expression and VIP release may be a necessary mechanism for the dopaminergic inhibition of PRL mRNA expression and PRL release.
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PMID:Autoparacrine action of vasoactive intestinal peptide on dopaminergic control of prolactin secretion. 859 96

The purpose of this study was to examine the role of vasoactive intestinal peptide (VIP) in prolactin (PRL) release in young turkey poults. Poults obtained from hens immunized with keyhole limpet hemocyanin (KLH)-chicken VIP (cVIP-KLH) conjugate or with KLH alone were used in this study. Plasma VIP antibody was tested by means of monoiodinated cVIP. Plasma samples were prediluted (1:100) in 0.05 EDTA PBS and used as a source of primary antibody in a cVIP-binding assay. Antibody levels averaged 50.8 +/- 10.3% at hatch and then declined with age to a level of 5.0 +/- 2.1% after 3 wk. Plasma PRL concentration was lower in cVIP-KLH-immunized poults (p < 0.05) than in KLH-immunized birds. Exogenous VIP administration at 7 days of age (7.8 micrograms/kg) increased plasma PRL level (p < 0.05) to a peak value of 359 +/- 32 ng/ml in the KLH-immunized birds. A smaller increase (p < 0.05) was obtained when the KLH-immunized poults received injections at 2 and 3 wk of age. The PRL response to cVIP administration was not observed in 1- and 2-wk-old poults maternally immunized with cVIP-KLH. Similarly, electrical stimulation of the ventromedial nucleus of the hypothalamus, at 1 and 8 days of age, induced a significant increase in the plasma PRL level of maternally KLH-immunized birds but not in maternally cVIP-KLH-immunized birds. These findings suggest that cVIP is a PRL-releasing factor in young turkey poults, similar to the finding in adult turkey hens.
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PMID:Effect of maternal passive immunization against vasoactive intestinal peptide on prolactin secretion in turkey poults. 883 90

Corneal infection with Pseudomonas aeruginosa perforates the cornea in susceptible C57BL/6 (B6), but not resistant BALB/c, mice. To determine whether vasoactive intestinal peptide (VIP) played a role in development of the resistant response, protein expression levels were tested by immunocytochemistry and enzyme immunoassay in BALB/c and B6 corneas. Both mouse strains showed constitutive expression of corneal VIP protein and nerve fiber distribution. However, disparate expression patterns were detected in the cornea after infection. VIP protein was elevated significantly in BALB/c over B6 mice at 5 and 7 days postinfection. Therefore, B6 mice were injected with rVIP and subsequently demonstrated decreased corneal opacity and resistance to corneal perforation compared with PBS controls. rVIP- vs PBS-treated B6 mice also demonstrated down-regulation of corneal mRNA and/or protein levels for proinflammatory cytokines/chemokines: IFN-gamma, IL-1beta, MIP-2, and TNF-alpha, whereas anti-inflammatory mediators, IL-10 and TGF-beta1, were up-regulated. Treatment with rVIP decreased NO levels and polymorphonuclear neutrophil (PMN) number. To further define the role of VIP, peritoneal macrophages (Mphi) and PMN from BALB/c and B6 mice were stimulated with LPS and treated with rVIP. Treatment of LPS-stimulated Mphi from both mouse strains resulted in decreased IL-1beta and MIP-2 protein levels; PMN responded similarly. Both cell types also displayed a strain-dependent differential response to rVIP, whereby B6 Mphi/PMN responded only to a higher concentration of VIP compared with cells from BALB/c mice. These data provide evidence that neuroimmune regulation of the cytokine network and host inflammatory cells functions to promote resistance against P. aeruginosa corneal infection.
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PMID:Vasoactive intestinal peptide balances pro- and anti-inflammatory cytokines in the Pseudomonas aeruginosa-infected cornea and protects against corneal perforation. 1720 74