VIP activation of rat anterior pituitary adenylate cyclase

Robberecht, Patrick; Deschodt-Lanckman, M; Camus, Jean Claude; Neef, Philippe De; Lambert, Monique; Christophe, Jean

doi:10.1016/0014-5793(79)81333-2

Cited by 82 publications

(58 citation statements)

References 16 publications

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“…(iii) For unknown reasons the brain cells are less sensitive to secretin than the pancreatic acinar cells are. In addition, their sensitivity to VIP is far below that of pancreatic acinar cells (25,30), fat cells (31), liver (31,32), intestinal epithelium (33), pituitary (34), and brain (35,36). In these cases the VIP receptors that are highly sensitive to VIP also display a low sensitivity to secretin, as derived from receptor binding studies (32,33,35,36) and measurements of adenylate cyclase (31,34) or of concentrations of cellular cyclic AMP (33,34).…”

Section: Discussionmentioning

confidence: 99%

Regulation by secretin, vasoactive intestinal peptide, and somatostatin of cyclic AMP accumulation in cultured brain cells.

Calker¹,

Müller²,

Hamprecht³

1980

Proc. Natl. Acad. Sci. U.S.A.

102

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Secretin stimulates the accumulation of cyclic AMP (half maximally stimulating concentration: 10-20 nM) in cultured mouse brain cells mainly consisting of glioblasts. Vasoactive Various peptides are known to be common to the brain and the gastrointestinal tract and pancreas (1). Some of these peptides (e.g., substance P, somatostatin, enkephalin) have been shown to elicit specific behavioral changes or changes in specific neuron firing rates or patterns (for review see refs. 2-4). They are, therefore, hypothesized to act on neurons as neuromodulators or neurotransmitters. Some neurohormones are also known to act on glial cells by regulating the intracellular level of cyclic AMP (for review see ref. 5). The possibility had to be considered that this would not only hold for biogenic amines such as norepinephrine but also for peptide hormones. Therefore, we investigated the effects of peptide hormones on the accumulation of cyclic AMP in glial cell cultures derived from neonatal mouse brain. We report-here that somatostatin inhibits the basal and the hormone-induced accumulation of cyclic AMP in such primary cultures. Furthermore, we report that the gastrointestinal hormones secretin and vasoactive intestinal peptide (VIP) stimulate the accumulation of cyclic AMP in these cultures, probably via different types of receptors. Thus a possible role of peptide hormones in the function of glial cells is indicated. In addition, the results suggest that secretin or a closely related compound might exert regulatory influence in the brain. A preliminary report of some of these results has been presented at a conference (6).MATERIALS AND METHODS Materials. Dulbecco's modified Eagle's medium and fetal bovine serum (GIBCO) were from C. Roth, Karlsruhe, Federal Republic of Germany. A partially purified preparation of VIP (porcine) was kindly donated by V. Mutt, Stockholm, Sweden. Isolated somatostatin (cyclic; bovine) was from Beckman,

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Section: Discussionmentioning

confidence: 99%

Regulation by secretin, vasoactive intestinal peptide, and somatostatin of cyclic AMP accumulation in cultured brain cells.

Calker¹,

Müller²,

Hamprecht³

1980

Proc. Natl. Acad. Sci. U.S.A.

102

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“…In previous studies, we demonstrated that VIP stimulates the proliferation of lactotroph cells in rats (Fernández et al 2003). The actions of VIP are mediated by activation of adenylate cyclase and the increase in intracellular cAMP levels (Robberecht et al 1979, Wanke & Rorstad 1990. Previous studies have provided evidence of an important role for cAMP not only in the regulation of lactotroph functions, such as secretion, synthesis and transcriptional regulation of PRL (Maurer 1981, Swennen & Denef 1982, Liang et al 1992, Romano et al 2003, but also in the proliferation of lactotrophs (Suzuki et al 1999).…”

Section: Introductionmentioning

confidence: 99%

IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

Fernández¹,

Sánchez‐Franco²,

Palacios³

et al. 2005

Journal of Molecular Endocrinology

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In previous studies we demonstrated that vasoactive intestinal peptide (VIP) mediation, and interactions between mitogen-activated protein kinase (MAPK) and cAMP/protein kinase A (PKA) signaling pathways are implicated in insulin-like growth factor I (IGF-I)-and VIP-induced lactotroph proliferation. These facts led us to investigate the intracellular mechanisms involved in IGF-I-and VIP-induced lactotroph proliferation. Exposure of cultured male rat pituitary cells to IGF-I (10 −7 M) or VIP (10 −7 M) stimulated the MAPK cascade. Studies in GH4C1 cells, with an expression vector for Rap1 GTPase-activating protein (Rap1 GAP1), demonstrated reduced VIP-induced MAPK activation, indicating that VIP-dependent activation of the extracellular signal-regulated kinase (ERK) pathway requires PKA-Rap1 signaling. IGF-I induced cAMP-response element (CRE)-binding protein (CREB) phosphorylation through the Ras-MAPK pathway, whereas VIP phosphorylated CREB directly via PKA. The mechanisms that regulate IGF-Iand VIP-CREB-dependent gene transcription were examined using GH4C1 cells transiently transfected with a CRE reporter gene. IGF-I and VIP stimulation of CRE-mediated transcription required activation of both Ras-MAPK and cAMP/PKA signaling. This activation was blocked in the presence of Rap1 GAP1. In summary, we showed that IGF-I and VIP stimulated MAPK activity and the phosphorylation of CREB in pituitary cells. Furthermore, VIP-dependent activation of PKA-Rap1-ERK pathways mediated VIP and IGF-I effects on CREB-dependent transcription in GH4C1 cells. Thus, it is possible that VIP-and IGF-I-induced lactotroph proliferation may involve Rap1.

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“…This concentration of cycloheximide did not modify basal or VIP-induced cAMP production but counteracted the inhibitory effect of Dex on VIP-induced cAMP accumulation ( Table 2). 10-14 10-13 [10][11][12] Dex, M gests that the effect of Dex is due to its glucocorticoid activity (Table 3). This conclusion is further substantiated by the observation that aldosterone had no effect under our experimental conditions.…”

Section: Methodsmentioning

confidence: 99%

“…In contrast, aldosterone, progesterone, estradiol, and testosterone have no effect. These results demonstrate that, in normal rat pituitary cells in culture, glucocorticoids at physiological concentrations rapidly inhibit the cAMP production and prolactin release induced by VIP by acting through specific glucocorticoid receptors.Vasoactive intestinal peptide (VIP) (9,10).In the light of both in vivo and in vitro experiments (6, 11), we suggested that corticosteroids could be involved in the regulation of VIP action on the adenohypophysis. We had previously shown that addition of dexamethasone (Dex) for 2 days to cultures of enriched pituitary rat lactotrophs completely abolished the stimulatory effect ofVIP on PRL secretion (6).…”

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Rapid glucocorticoid inhibition of vasoactive intestinal peptide-induced cyclic AMP accumulation and prolactin release in rat pituitary cells in culture.

Rotsztejn¹,

Dussaillant²,

Nobou³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

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Vasoactive intestinal peptide (VIP) stimulates both adenosine 3',5'-cyclic monophosphate (cAMP) accumulation and prolactin release in normal rat pituitary cells in culture. cAMP accumulation is significant (P < 0.01) at VIP concentrations as low as 1 nM and reaches a maximum with 0.1 ,IM. Addition of dexamethasone as early as 15 min before VIP inhibits VIP stimulation of both cAMP production and PRL secretion. The rapid inhibition is dose-dependent: it appears at doses as low as 0.01 pM and is complete at 1 pM dexamethasone. Increasing concentrations of dexamethasone induce a noncompetitive type of inhibition, as shown by the decrease in Vm.,. with no change in the apparent K.for VIP. Cycloheximide (1 mM) counteracts the inhibitory effect of dexamethasone on VIP-induced cAMP production, which suggests the involvement ofa rapid protein synthesis mechanism. Ru-26988, a specific glucocorticoid devoid of any mineralocorticoid activity and which does not bind to intracellular transcortin-like component, also produces an inhibition of VIP-induced cAMP accumulation. Corticosterone also inhibits VIP-induced cAMP production but at concentrations higher than those ofdexamethasone. In contrast, aldosterone, progesterone, estradiol, and testosterone have no effect. These results demonstrate that, in normal rat pituitary cells in culture, glucocorticoids at physiological concentrations rapidly inhibit the cAMP production and prolactin release induced by VIP by acting through specific glucocorticoid receptors.Vasoactive intestinal peptide (VIP) (9,10).In the light of both in vivo and in vitro experiments (6, 11), we suggested that corticosteroids could be involved in the regulation of VIP action on the adenohypophysis. We had previously shown that addition of dexamethasone (Dex) for 2 days to cultures of enriched pituitary rat lactotrophs completely abolished the stimulatory effect ofVIP on PRL secretion (6). Therefore, we have investigated (a) the involvement of the cAMP system in the biological effect of VIP on PRL release, (b) the kinetics and the stoichiometry of the interaction between VIP and corticosteroids, and (c) the mechanism by which Dex inhibits PRL release at the pituitary level.In the present communication, we present evidence that, in normal rat pituitary cells in culture, Dex at concentrations as low as 1 pM rapidly inhibits both the cAMP accumulation and the PRL release induced by VIP, by acting through specific glucocorticoid receptors. MATERIALS AND METHODSIsolation and Cell Culture. Male Wistar rats (45-60 days old) were used. Fifteen to 20 anterior pituitaries were minced in small pieces and dispersed enzymatically by incubation in 15-20 ml of minimal essential medium with Earle's salts containing 0.1% trypsin (1:250) (GIBCO) and 0.1% fatty acid-free bovine serum albumin (Sigma) for 2 hr at 370C (12) at pH 7.5 in a silicone-treated Bellco spinner flask. Cells were filtered though 100-,um-mesh nylon to remove DNA of broken cells and centrifuged at 400 g for 5 min; the pellet was resuspended, w...

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VIP activation of rat anterior pituitary adenylate cyclase

Cited by 82 publications

References 16 publications

Regulation by secretin, vasoactive intestinal peptide, and somatostatin of cyclic AMP accumulation in cultured brain cells.

Regulation by secretin, vasoactive intestinal peptide, and somatostatin of cyclic AMP accumulation in cultured brain cells.

IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

Rapid glucocorticoid inhibition of vasoactive intestinal peptide-induced cyclic AMP accumulation and prolactin release in rat pituitary cells in culture.

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