VIP Activates Gs and Gi3 in Rat Alveolar Macrophages and Gs in HEK293 Cells Transfected with the Human VPAC1 Receptor

Shreeve, S. Martin; Sreedharan, Sunil P.; Hacker, Miles P.; Gannon, David; Morgan, Matthew J.

doi:10.1006/bbrc.2000.2879

Cited by 17 publications

(8 citation statements)

References 40 publications

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“…The molecular basis for the cAMP-independent pathway remains to be established. VIP was shown to activate both ␣s and ␣i3 G proteins in rat alveolar macrophages (Shreeve et al, 2000). Whether the ␣i3 G protein could account for the cAMP-independent pathway in murine peritoneal macrophages remains to be determined.…”

Section: Vasoactive Intestinal Peptide Signalingmentioning

confidence: 97%

“…VPAC receptors induce responses by activating transduction systems that involve different G-proteins, with G␣ as the best characterized in different tissues and cell lines expressing recombinant receptors. Others G proteins that have been shown to be coupled to VPAC receptors belong to Gi/Go and Gq families (Pozo et al, 1997a;Van Rampelbergh et al, 1997;McCulloch et al, 2000;Shreeve et al, 2000;MacKenzie et al, 2001). Also, other VPAC partners different of G proteins have been reported, such as the small G-protein ADP-ribosylation factor (McCulloch et al, 2001) or receptor activity-modifying proteins (Christopoulos et al, 2003), resulting in alterations of receptor phenotype or pharmacological profile (McLatchie et al, 1998).…”

Section: B Biochemical Pharmacological and Signaling Key Features mentioning

confidence: 99%

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The Significance of Vasoactive Intestinal Peptide in Immunomodulation

Delgado

Pozo²,

Ganea³

2004

Pharmacol Rev

372

319

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Section: Vasoactive Intestinal Peptide Signalingmentioning

confidence: 97%

Section: B Biochemical Pharmacological and Signaling Key Features mentioning

confidence: 99%

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

Delgado

Pozo²,

Ganea³

2004

Pharmacol Rev

372

319

View full text Add to dashboard Cite

“…However, VIP-induced, cAMP-independent pathways have also been reported. This was based on the fact that H89, a specific PKA inhibitor, was not effective in blocking some VIP-induced effects [11,17,26]. These reports were not taking into account that cAMP-dependent/PKA-independent pathways could also play a role in VIP effects.…”

Section: Introductionmentioning

confidence: 99%

VIP differentially activates β2 integrins, CR1, and matrix metalloproteinase-9 in human monocytes through cAMP/PKA, EPAC, and PI-3K signaling pathways via VIP receptor type 1 and FPRL1

Zein

Badran

Sariban

2008

Journal of Leukocyte Biology

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The neuropeptide vasoactive intestinal peptide (VIP) regulates the exocytosis of secretory granules in a wide variety of cells of neuronal and non-neuronal origin. In human monocytes, we show that the proinflammatory effects of VIP are associated with stimulation of exocytosis of secretory vesicles as well as tertiary (gelatinase) granules with, respectively, up-regulation of the membrane expression of the beta2 integrin CD11b, the complement receptor 1 (CD35), and the matrix metalloproteinase-9 (MMP-9). Using the low-affinity formyl peptide receptor-like 1 (FPRL1) antagonist Trp-Arg-Trp-Trp-Trp-Trp (WRW4) and the exchange protein directly activated by cAMP (EPAC)-specific compound 8CPT-2Me-cAMP and measuring the expression of Rap1 GTPase-activating protein as an indicator of EPAC activation, we found that the proinflammatory effect of VIP is mediated via the specific G protein-coupled receptor VIP/pituitary adenylate cyclase-activating protein (VPAC1) receptor as well as via FPRL1: VIP/VPAC1 interaction is associated with a cAMP increase and activation of a cAMP/p38 MAPK pathway, which regulates MMP-9, CD35, and CD11b exocytosis, and a cAMP/EPAC/PI-3K/ERK pathway, which regulates CD11b expression; VIP/FPRL1 interaction results in cAMP-independent PI-3K/ERK activation with downstream integrin up-regulation. In FPRL1-transfected Chinese hamster ovary-K1 cells lacking VPAC1, VIP exposure also resulted in PI-3K/ERK activation. Thus, the proinflammatory effects of VIP lie behind different receptor interactions and multiple signaling pathways, including cAMP/protein kinase A, cAMP/EPAC-dependent pathways, as well as a cAMP-independent pathway, which differentially regulates p38 and ERK MAPK and exocytosis of secretory vesicles and granules.

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“…VIP is the most abundant peptide in the airways and the VPAC 1 receptor has been shown to stimulate CFTR-dependent chloride secretion upon VIP binding through activation of both PKA-and PKC-dependent signaling pathways in airway submucosal glands epithelial cell line Calu-3 (Chappe et al, 2008;Derand et al, 2004). Although class II GPCR are generally coupled to G s 2 and adenylate cyclase activation to increase intracellular cAMP content, numerous reports have demonstrated that VIP receptors can couple to alternate G proteins and elicit signaling cascades cross-talk involving G i/q 2 , PKC and calcium release on top of the conventional G s and cAMP cascade (Derand et al, 2004;Bewley et al, 2006;Chappe et al, 2008;Sreedharan et al, 1994;Xia et al, 1996;Shreeve et al, 2000;Rafferty et al, 2009) (Fig. 3).…”

Section: Regulation Of Cftr Activation By Vip Acute Stimulationmentioning

confidence: 99%