Activation of Pituitary Adenylate Cyclase-Activating Polypeptide Receptors Prevents Apoptotic Cell Death in Cultured Cerebellar Granule Cellsa

Canonico, Pier Luigi; Copani, Agata; D’Agata, Velia; Musco, Simone; Petralia, Salvatore; Travali, Salvatore; Stivala, Franca; Cavallaro, Sebastiano

doi:10.1111/j.1749-6632.1996.tb17505.x

Cited by 30 publications

(20 citation statements)

References 7 publications

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“…Indeed, PACAP exerts neurotrophic activities on many cell types (Yuhara et al, 2001;Erhardt and Sherwood, 2004;Nielsen et al, 2004;Reglodi et al, 2004;Reglödi et al, 2006;Shioda et al, 2006). In cerebellar granule cells cultured in conditions promoting apoptosis, PACAP inhibits programmed cell death (Campbell and Scanes, 1992;Canonico et al, 1996;Cavallaro et al, 1996;Chang et al, 1996;Gonzalez et al, 1997;Villalba et al, 1997) and stimulates neurite outgrowth (Fig. 9) (Gonzalez et al, 1997).…”

Section: Actions Of Pituitary Adenylate Cyclase-activating Polypeptidmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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Section: Actions Of Pituitary Adenylate Cyclase-activating Polypeptidmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…Its survival-promoting effects were first described in neuronal cells, in chicken spinal cord, and cerebellar granule cells (Arimura et al 1994;Canonico et al 1996;Gonzalez et al 1997). Subsequently, dozens of reports have demonstrated its strong neuroprotective actions both in vitro and in vivo (Somogyvari-Vigh and Reglodi 2004;Vaudry et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Effects of PACAP on Oxidative Stress-Induced Cell Death in Rat Kidney and Human Hepatocyte Cells

et al. 2010

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Oxidative stress plays an important role in various renal and hepatic pathologies, and reduction of oxidative stress-induced processes is an important protective strategy in tissues of diverse origins against harmful stimuli. Pituitary adenylate cyclase activating polypeptide (PACAP) is a well-known cytotrophic and cytoprotective peptide. PACAP promotes cell survival in numerous cells and tissues exposed to various stimuli. Protective effects of PACAP have been shown in the kidney, but it is not known whether PACAP is protective against oxidative stress in renal cells. Little is known about the effects of PACAP in the liver. The aim of the present study was to investigate whether PACAP is protective against oxidative stress in primary rat kidney cell culture and whether PACAP has any effect on cell survival in human WRL-68 hepatocytes and HEP-G2 hepatocellular carcinoma cells subjected to oxidative stress. Cells were exposed to various concentrations of H(2)O(2) with or without PACAP co-treatment and cell viability was evaluated with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide test (MTT). We found that oxidative stress induced a significant decrease in cell viability in both cell lines. PACAP could dose-dependently increase the percentage of living cells in kidney cells, but it failed to do so in hepatocytes. Given the survival-promoting effects of PACAP against oxidative stress in rat kidney, we conducted a further experiment to determine whether PACAP influences the markers of oxidative stress in vivo. We have proven earlier that PACAP was effective in kidney ischemia/reperfusion injury in vivo. In the present study, we determined the levels of the oxidative stress marker malondialdehyde and the activity of the scavenger molecules glutathione (GSH) and superoxide dismutase (SOD) following kidney ischemia/reperfusion in rats. We found that PACAP significantly increased the level of GSH and counteracted the marked reduction of SOD activity after ischemia/reperfusion in vivo. In summary, the present study showed that while PACAP was able to significantly increase the cell survival in primary kidney cell cultures exposed to oxidative stress, possibly involving interaction with the endogenous scavenger system, it failed to influence the viability of normal or cancerous hepatocytes.

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“…In fact, PACAP has significant neurotrophic and neuroprotective effects in brain damage models in vivo [13,14] and in vitro [15][16][17][18][19]. PACAP prevents the ischemic death of rat CA1 neurons when given either intracerebroventricularly or intravenously in a model of transient global ischemia, even if administration is delayed for 24 h after the ischemic event [13].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection by endogenous and exogenous PACAP following stroke

Chen¹,

Samal²,

Hamelink³

et al. 2006

Regulatory Peptides

105

113

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We investigated the effects of PACAP treatment, and endogenous PACAP deficiency, on infarct volume, neurological function, and the cerebrocortical transcriptional response in a mouse model of stroke, middle cerebral artery occlusion (MCAO). PACAP-38 administered i.v. or i.c. v. 1 h after MCAO significantly reduced infarct volume, and ameliorated functional motor deficits measured 24 h later in wild-type mice. Infarct volumes and neurological deficits (walking faults) were both greater in PACAP-deficient than in wild-type mice, but treatment with PACAP reduced lesion volume and neurological deficits in PACAP-deficient mice to the same level of improvement as in wild-type mice.A 35,546-clone mouse cDNA microarray was used to investigate cortical transcriptional changes associated with cerebral ischemia in wild-type and PACAP-deficient mice, and with PACAP treatment after MCAO in wild-type mice. 229 known (named) transcripts were increased (228) or decreased (1) in abundance at least 50% following cerebral ischemia in wild-type mice. 49 transcripts were significantly up-regulated only at 1 h post-MCAO (acute response transcripts), 142 were up-regulated only at 24 h post-MCAO (delayed response transcripts) and 37 transcripts were up-regulated at both times (sustained response transcripts). More than half of these are transcripts not previously reported to be altered in ischemia.A larger percentage of genes up-regulated at 24 hr than at 1 hr required endogenous PACAP, suggesting a more prominent role for PACAP in later response to injury than in the initial response. This is consistent with a neuroprotective role for PACAP in late response to injury, i.e., even when administered 1 hr or more after MCAO. Putative injury effector transcripts regulated by PACAP include β-actin, midline 2, and metallothionein 1. Potential neuroprotective transcripts include several demonstrated to be PACAP-regulated in other contexts. Prominent among these ☆ Data deposition: The raw data from the expression profiling experiments reported in this paper have been deposited in the Gene Expression Omnibus database (accession no. GSE5902). The GSE5902 will be hyperlinked when it is released. were transcripts encoding the PACAP-regulated gene Ier3, and the neuropeptides enkephalin, substance P (tachykinin 1), and neurotensin.

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Activation of Pituitary Adenylate Cyclase-Activating Polypeptide Receptors Prevents Apoptotic Cell Death in Cultured Cerebellar Granule Cellsa

Cited by 30 publications

References 7 publications

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Effects of PACAP on Oxidative Stress-Induced Cell Death in Rat Kidney and Human Hepatocyte Cells

Neuroprotection by endogenous and exogenous PACAP following stroke

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