Effects of PACAP and VIP on hyperglycemia-induced proliferation in murine microvascular endothelial cells

Castorina, Alessandro; Giunta, Salvatore; Mazzone, Venera; Cardile, Venera; D’Agata, Velia

doi:10.1016/j.peptides.2010.08.013

Cited by 44 publications

(27 citation statements)

References 33 publications

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“…This PACAP effect is correlated with the increase of vascular endothelial growth factor C expression (fold change=66.7) in line with previous work, showing indirect PACAP-mediated control of endothelial cell proliferation through the induction of vascular endothelial growth factor production. 26,27 Because CD11b + cells represent the major source of vascular endothelial growth factor C in the brain parenchyma, 28 our data indicate that the beneficial effects of delayed PACAP delivery could rely on PACAP-induced vascular endothelial growth factor C-producing microglia/macrophages, thus promoting postischemic neovascularization. This hypothesis is reinforced by the increased Arg-1 labeling in vessel-like structures, illustrating an increased neoangiogenesis in ES-P cell-transplanted mice specifically.…”

Section: Strokementioning

confidence: 88%

Delayed Pituitary Adenylate Cyclase–Activating Polypeptide Delivery After Brain Stroke Improves Functional Recovery by Inducing M2 Microglia/Macrophage Polarization

Brifault

Gras

Liot

et al. 2015

Stroke

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520S troke is a leading cause of death and long-term disabilities worldwide. Despite years of intense research and preclinical identification of numerous potential neuroprotective compounds, the only available treatment for brain ischemia relies on thrombolysis through injection of a recombinant tissuetype plasminogen activator. However, the treatment benefits to <10% of stroke victims because of a narrow therapeutical time window (<4.5 hours after stroke onset) and side effects. Consequently, there is a crucial need for the development of other strategies that could target later phases of the pathophysiological cascade of events after stroke.Since its initial discovery, several studies have highlighted the neuroprotective effect of pituitary adenylate cyclase-activating polypeptide (PACAP) 2 in in vitro and in vivo models of neurodegenerative diseases.3,4 Administered either before or few hours after middle cerebral artery occlusion, PACAP reduces the infarct volume area and improves functional outcomes. [5][6][7] Beside its well-known antiapoptotic activity, the neuropeptide PACAP exerts potent anti-inflammatory properties on innate immune compartment as illustrated by the decrease of the production of proinflammatory mediators interleukin (IL)-12, tumor necrosis factor (TNF)-α, and nitric oxide and the induction of the anti-inflammatory cytokine IL-10 in PACAP-treated macrophages stimulated by lipopolysaccharides.8-10 Whether PACAP acts directly by reducing apoptotic neuronal death 11 or indirectly via modulation of Background and Purpose-Until now, except thrombolysis, the therapeutical strategies targeting the acute phase of cerebral ischemia have been proven ineffective, and no approach is available to attenuate the delayed cell death mechanisms and the resulting functional deficits in the late phase. Then, we investigated whether a targeted and delayed delivery of pituitary adenylate cyclase-activating polypeptide (PACAP), a peptide known to exert neuroprotective activities, may dampen delayed pathophysiological processes improving functional recovery. Methods-Three days after permanent focal ischemia, PACAP-producing stem cells were transplanted intracerebroventricularly in nonimmunosuppressed mice. At 7 and 14 days post ischemia, the effects of this stem cell-based targeted delivery of PACAP on functional recovery, volume lesions, and inflammatory processes were analyzed. Results-The

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Section: Strokementioning

confidence: 88%

Delayed Pituitary Adenylate Cyclase–Activating Polypeptide Delivery After Brain Stroke Improves Functional Recovery by Inducing M2 Microglia/Macrophage Polarization

Brifault

Gras

Liot

et al. 2015

Stroke

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“…PACAP exerts neuroprotective (Tsuchikawa et al 2012 ), cytoprotective, pro-survival (Brown et al 2013 ), anti-inflammatory, vasodilator, and several other effects (for review see: Vaudry et al 2009 ;Reglodi et al 2012 ). PACAP has been shown to have several effects on microvascular endothelia of non-cerebral origin: it protects mouse hemangioendothelioma cells against the apoptosis-inducing effects of oxidative stress (Racz et al 2007 ) and inhibits hyperglycemia-induced proliferation in H5V murine microvascular endothelial cells (Castorina et al 2010 ). However, the effects of PACAP on brain endothelial cells are incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

PACAP Enhances Barrier Properties of Cerebral Microvessels

et al. 2014

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Cerebral microvascular endothelial cells-coming in contact with pericytes and astrocytes-constitute the structural basis of the blood-brain barrier (BBB). The continuous belt of interendothelial tight junctions (TJs) and the presence of specific transport systems, enzymes, and receptors in the brain endothelium regulate the molecular and cellular traffic into the central nervous system. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide having several cellular protective effects. However, little is known about the effects of PACAP on the cerebral endothelium and BBB functions. Here, we show that PACAP has no significant pro-survival role in cerebral microvascular endothelial cells;

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“…Tsutsumi et al (2002) described that activation of VPAC1-R has been implicated in elevating glucose output, whereas activation of VPAC2-R may be involved in insulin secretion. PACAP exerts an inhibitory activity on hyperglycemia-induced endothelial cell proliferation, thus suggesting that the effect might be mediated by PAC1 and VPAC2 receptors (Castorina et al, 2010). We have also found unusual cells, like pericytes, granulocytes, and macrophages, in PACAP-treated diabetic retina .…”

Section: P1025mentioning

confidence: 51%

“…It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication.hyperglycemia-induced microvascular endothelial cell growth in vitro (Castorina et al, 2010). …”

mentioning

confidence: 99%

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Szabadfi

Pintér

Reglődi

et al. 2014

International Review of Cell and Molecular Biology

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Any queries or remarks that have arisen during the processing of your manuscript are listed below and are highlighted by flags in the proof. (AU indicates author queries; ED indicates editor queries; and TS/TY indicates typesetter queries.) Please check your proof carefully and answer all AU queries. Mark all corrections and query answers at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file http:// www.elsevier.com/book-authors/science-and-technology-book-publishing/overviewof-the-publishing-process) or compile them in a separate list, and tick off below to indicate that you have answered the query. Please return your input as instructed by the project manager. Location in ChapterQuery / remark AU:1, page 47 Please check the change made in the table title. AU:2, page 57 Citation " Frank et al. (1997)" has not been found in the reference list. Please supply full details for this reference. AU:3, page 58Citation "Wang et al. (2004)" has not been found in the reference list. Please supply full details for this reference. AU:4, page 63The citation "Wang et al. (2010)" has been changed to " Wang et al. (2010)" to match the author name/date in the reference list. Please check here and in subsequent occurrences, and correct if necessary. AU:5, page 3The abbreviations IBA-1 and ZFDM are used only once in the text and they have been deleted in the text. Please consider deleting them from the abbreviation list. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:6, page 3Please check if all occurrences of "interstitial cell adhesion molecule 1" should be changed to "intercellular adhesion molecule 1." AU:7, page 3Please check the change from "neural" to "neuronal" to match with the text.AU:8, page 3The abbreviation "PKCa" is not used in the text. Please check and delete from the abbreviation list. AU:9, page 9Please check if "retinal ganglion cells (RGCs)" is okay as edited.AU:10, page 13 Please check the change from "retinal circuity" to "retinal circuitry."AU:11, page 17 Please check if "polyamine catabolism" is okay as edited. AU:20, page 46 Please check if edit to sentence starting "The STZ-induced diabetic. . ." is okay. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:21, page 72Please check if "SST" is okay as edited.AU:2...

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Effects of PACAP and VIP on hyperglycemia-induced proliferation in murine microvascular endothelial cells

Cited by 44 publications

References 33 publications

Delayed Pituitary Adenylate Cyclase–Activating Polypeptide Delivery After Brain Stroke Improves Functional Recovery by Inducing M2 Microglia/Macrophage Polarization

Delayed Pituitary Adenylate Cyclase–Activating Polypeptide Delivery After Brain Stroke Improves Functional Recovery by Inducing M2 Microglia/Macrophage Polarization

PACAP Enhances Barrier Properties of Cerebral Microvessels

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

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