PACAP and VIP increase the expression of myelin-related proteins in rat schwannoma cells: Involvement of PAC1/VPAC2 receptor-mediated activation of PI3K/Akt signaling pathways

Castorina, Alessandro; Scuderi, Soraya; D’Amico, Agata Grazia; Drago, Filippo; D’Agata, Velia

doi:10.1016/j.yexcr.2013.11.003

Cited by 50 publications

(50 citation statements)

References 42 publications

(54 reference statements)

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“…The broad spectrum PKC inhibitor Ro 318220 inhibited PACAP-27-induced TG2 activity, indicating that Gq-protein coupling is involved in PAC1 receptor-mediated TG2 activation. The PAC1 receptor also activates ERK1/2, JNK1/2, p38 MAPK and PKB (Monaghan et al, 2008;May et al, 2010, Castorina et al, 2014. In this study we observed PACAP-27-induced activation of ERK1/2, JNK1/2, and PKB but not p38 MAPK.…”

Section: Role Of Protein Kinases In Pac1 Receptor-mediated Tg2 Activasupporting

confidence: 54%

“…The PAC1 receptor is a member of the GPCR superfamily which activates adenylyl cyclase/cAMP/PKA (via Gsprotein coupling) and phospholipase C/DAG/PKC (via Gq-protein coupling) dependent signalling pathways (Dickson and Finlayson, 2009;Vaudry et al, 2009). The PAC1 receptor also triggers the activation of several other protein kinase cascades such as ERK1/2, JNK1/2, p38 MAPK and PKB (Monaghan et al, 2008;May et al, 2010, Castorina et al 2014. Since some of these protein kinase pathways are associated with modulation of TG activity (PKA, PKC and ERK1/2) it is conceivable that the PAC1 receptor regulates TG activity.…”

Section: Introductionmentioning

confidence: 99%

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Role of transglutaminase 2 in PAC1 receptor mediated protection against hypoxia-induced cell death and neurite outgrowth in differentiating N2a neuroblastoma cells

Algarni

Hargreaves

Dickenson

2017

Biochemical Pharmacology

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Section: Role Of Protein Kinases In Pac1 Receptor-mediated Tg2 Activasupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Role of transglutaminase 2 in PAC1 receptor mediated protection against hypoxia-induced cell death and neurite outgrowth in differentiating N2a neuroblastoma cells

Algarni

Hargreaves

Dickenson

2017

Biochemical Pharmacology

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“…In mammals, PAC-I receptors are known to couple with MAPK signaling via cAMP-dependent (Monaghan et al 2008) and/or independent pathways (Hamelink et al 2002, Vaudry et al 2003. In addition, PACAP activation of the PI3K/Akt pathway via the PAC1/VPAC2 receptors has also been reported, for example, in rat schwannoma cells (Castorina et al 2014). In grass carp pituitary cells, however, PACAP-induced prl mRNA expression was not sensitive to MEK 1/2 inhibition by U0126, P 38 MAPK blockade with PD16316, or PI3K inactivation using Ly294002.…”

Section: :1mentioning

confidence: 99%

Mechanisms for PACAP-induced prolactin gene expression in grass carp pituitary cells

Lin

Jiang

et al. 2017

Journal of Endocrinology

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In mammals, pituitary adenylate cyclase-activating polypeptide (PACAP) is a pleiotropic hormone with diverse functions but its role in prolactin (PRL) regulation is highly controversial. To shed light on Prl regulation by PACAP in fish model, grass carp pituitary cells was used as a model to examine the receptor specificity and signal transduction for PACAP modulation of gene expression in the carp pituitary. Using RT-PCR, PACAP-selective PAC1 receptor was detected in carp lactotrophs. In carp pituitary cells, nanomolar doses of PACAP, but not VIP, could elevate Prl secretion and protein production with concurrent rise in mRNA and these stimulatory effects were blocked by PACAP antagonist but not VIP antagonist. PACAP-induced mRNA expression could be mimicked by activating adenylate cyclase (AC), increasing cAMP level by cAMP analog, or increasing intracellular Ca ([Ca]i) by Ca ionophore/voltage-sensitive Ca channel (VSCC) activator. PACAP-induced gene expression, however, was attenuated/abolished by suppressing cAMP production, inhibiting PKA activity, blocking [Ca]i mobilization and VSCC activation, calmodulin (CaM) antagonism, and inactivation of JNK and CaM Kinase II (CaMK-II). Similar sensitivity to CaM, JNK, and CaMK-II blockade was also noted by substituting cAMP analog for PACAP as the stimulant for mRNA expression. These results, as a whole, provide evidence for the first time that (i) PACAP activation of PAC1 receptor expressed in carp lactotrophs could induce Prl synthesis and secretion, and (ii) Prl production induced by PACAP was mediated by upregulation of gene expression, presumably via functional coupling of cAMP/PKA-, Ca/CaM-, and MAPK-dependent cascades.

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“…Among neuropeptides displaying protective role in DR, pituitary adenylyl cyclase‐activating polypeptide (PACAP) has been also included (Cavallaro et al, ; Danyadi et al, ; D'Agata & Cavallaro, ; D'Agata, Cavallaro, Stivala, & Canonico, ; Fabian et al, ; Gábriel, ; Giunta et al, , ; Scuderi et al, ). In particular, it is able to interfere with apoptotic process affecting tissues and cells besides hypoxia occurring in DR by modulating retinal HIFs expression and preventing outer BRB breakdown (Castorina et al, ; Castorina, Giunta, et al, ; Castorina, Scuderi, D'Amico, Drago, & D'Agata, ; D'Amico et al, ; Maugeri, D'Amico, Gagliano, et al, ; Maugeri, D'Amico, Saccone, et al, ).…”

Section: Introductionmentioning

confidence: 99%

NAP counteracts hyperglycemia/hypoxia induced retinal pigment epithelial barrier breakdown through modulation of HIFs and VEGF expression

D’Amico

Maugeri

Rasà

et al. 2017

Journal Cellular Physiology

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Diabetic macular edema (DME) is a common complication leading to a central vision loss in patients with diabetes. In this eye pathology, the hyperglycaemic/hypoxic microenvironment of pigmented epithelium is responsible for outer blood retinal barrier integrity changes. More recently, we have shown that a small peptide derived from the activity-dependent neuroprotective protein (ADNP), known as NAP, counteracts damages occurring during progression of diabetic retinopathy by modulating HIFs/VEGF pathway. Here, we have investigated for the first time the role of this peptide on outer blood retinal barrier (BRB) integrity exposed to hyperglycaemic/hypoxic insult mimicking a model in vitro of DME. To characterize NAP role on disease's pathogenesis, we have analyzed its effect on HIFs/VEGF system in human retinal pigmented epithelial cells, ARPE-19, grown in high glucose and low oxygen tension. The results have shown that NAP prevents outer BRB breakdown by reducing HIF1α/HIF2α, VEGF/VEGFRs, and increasing HIF3α expression, moreover it is able to reduce the percentage of apoptotic cells by modulating the expression of two death related genes, BAX and Bcl2. Further investigations are needed to determine the possible use of NAP in DME treatment.

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PACAP and VIP increase the expression of myelin-related proteins in rat schwannoma cells: Involvement of PAC1/VPAC2 receptor-mediated activation of PI3K/Akt signaling pathways

Cited by 50 publications

References 42 publications

Role of transglutaminase 2 in PAC1 receptor mediated protection against hypoxia-induced cell death and neurite outgrowth in differentiating N2a neuroblastoma cells

Role of transglutaminase 2 in PAC1 receptor mediated protection against hypoxia-induced cell death and neurite outgrowth in differentiating N2a neuroblastoma cells

Mechanisms for PACAP-induced prolactin gene expression in grass carp pituitary cells

NAP counteracts hyperglycemia/hypoxia induced retinal pigment epithelial barrier breakdown through modulation of HIFs and VEGF expression

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