Ameliorative effect of PACAP and VIP against increased permeability in a model of outer blood retinal barrier dysfunction

Scuderi, Soraya; D’Amico, Agata Grazia; Castorina, Alessandro; Imbesi, Rosa; Carnazza, Maria Luisa; D’Agata, Velia

doi:10.1016/j.peptides.2012.11.015

Cited by 50 publications

(49 citation statements)

References 35 publications

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“…Occludin expression was not affected in any of the conditions tested. Altogether, these fi ndings show that both peptides counteract high glucose + IL-1β-induced damage in ARPE19 cells, suggesting that they might be relevant to the maintenance of outer blood-retinal barrier function in edema accompanying diabetic retinopathy [ 55 ]. These results are in accordance with our earlier observations in an in vitro blood-brain barrier (BBB) model [ 56 ].…”

Section: In Vitro Protective Effects In the Retinal Pigment Epitheliasupporting

confidence: 91%

“…Another study investigated the potential of PACAP and VIP against the disruption of tight junctions in the retina, a major factor in macular edema developing in diabetic retinopathy [ 55 ]. ARPE19 cells were cultured either in normal glucose or in high glucose in combination with the pro-infl ammatory IL-1β.…”

Section: In Vitro Protective Effects In the Retinal Pigment Epitheliamentioning

confidence: 99%

“…ARPE19 cells were cultured either in normal glucose or in high glucose in combination with the pro-infl ammatory IL-1β. Effects on permeability were evaluated by measuring both apical-to-basolateral movements of fl uorescein isothiocyanate (FITC) dextran and transepithelial electrical resistance [ 55 ]. Results of these experiments demonstrated that normal glucose + IL-1β and, to a greater extent, high glucose + IL-1β signifi cantly increased FITC-dextran diffusion, paralleled by decreased electrical resistance.…”

Section: In Vitro Protective Effects In the Retinal Pigment Epitheliamentioning

confidence: 99%

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Protective Effects of PACAP in the Retina

Atlasz

Vaczy

Werling

et al. 2016

Current Topics in Neurotoxicity

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Pituitary adenylate cyclase activating polypeptide (PACAP) is a widespread neuropeptide that is well known for its general cytoprotective effects in different neuronal injuries, such as traumatic brain and spinal cord injury, models of neurodegenerative diseases, and cerebral ischemia. PACAP and its receptors also occur in the retina. In this review, we summarize the retinoprotective effects of PACAP. In vitro, PACAP is protective against glutamate, thapsigargin, anisomycin, oxidative stress, UV light, high glucose, infl ammation, and anoxia. Both the neural retina and the pigment epithelial cells can be protected by PACAP in various experimental paradigms. In vivo, the protective effects of intravitreal PACAP treatment have been shown in the following models in rats and mice: excitotoxic injury induced by glutamate, N -methyl-D -aspartate (NMDA) or kainate, ischemic injury induced by carotid artery ligation and high intraocular pressure, degeneration caused by UV-A light, optic nerve transection, and streptozotocin-induced diabetic retinopathy as well as retinopathy of prematurity. Molecular biological methods have revealed that PACAP activates anti-apoptotic, while inhibits pro-apoptotic signaling pathways, and it also stimulates an anti-infl ammatory environment in the retina. Altogether, PACAP is suggested to be a potential therapeutic retinoprotective agent in various retinal diseases.

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Section: In Vitro Protective Effects In the Retinal Pigment Epitheliasupporting

confidence: 91%

Section: In Vitro Protective Effects In the Retinal Pigment Epitheliamentioning

confidence: 99%

Section: In Vitro Protective Effects In the Retinal Pigment Epitheliamentioning

confidence: 99%

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Protective Effects of PACAP in the Retina

Atlasz

Vaczy

Werling

et al. 2016

Current Topics in Neurotoxicity

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“…This process was reversed by PACAP and VIP. Both peptides counteract hyperglycemia-induced damage in ARPE-19 cells, suggesting that they might be relevant to the maintenance of outer BRB function (Scuderi et al, 2013). …”

mentioning

confidence: 94%

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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“…Moreover, in diabetic macular edema, activation of the protective VIP/PACAP pathway has been shown to prevent the breakdown of the outer blood retinal barrier by mediating tight junction integrity 16 . However, the modulatory mechanism and potential therapeutic effect of VIP during the development of DR is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

VIP protects human retinal microvascular endothelial cells against high glucose-induced increases in TNF-α and enhances RvD1

Shi

Carion

Jiang

et al. 2016

Prostaglandins & Other Lipid Mediators

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Purpose The purpose of our study was to evaluate the therapeutic effect of VIP on human retinal endothelial cells (HREC) under high glucose conditions. Diabetes affects almost 250 million people worldwide. Over 40% of diabetics are expected to develop diabetic retinopathy, which remains the leading cause of visual impairment/blindness. Currently, treatment is limited to late stages of retinopathy with no options available for early stages. To this end, the purpose of the current study is to evaluate the therapeutic effect of vasoactive intestinal peptide (VIP) on HREC under high glucose conditions. Methods Primary HREC were cultured in normal (5 mM) or high (25 mM) glucose medium +/− VIP treatment. Protein levels of TNF-α, resolvin D1 (RvD1), formyl peptide receptor 2 (FPR2), G protein-coupled receptor 32 (GPR32), VEGF, and VIP receptors, VPAC1 and VPAC2 were measured. Results High glucose-induced changes in TNF-α and RvD1 were restored to control levels with VIP treatment. RvD1 receptors, FPR2 and GPR32, were partially rescued with VIP treatment. VPAC2 expression appeared to be the major receptor involved in VIP signaling in HREC, as VPAC1 receptor was not detected. In addition, VIP did not induce HREC secretion of VEGF under high glucose conditions. Conclusions Our results demonstrate that VIP’s therapeutic effect on HREC, occurs in part, through the balance between the pro-inflammatory cytokine, TNF-α, and the pro-resolving mediator, RvD1. Although VPAC1 is considered the major VIP receptor, VPAC2 is predominantly expressed on HREC under both normal and high glucose conditions.

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Ameliorative effect of PACAP and VIP against increased permeability in a model of outer blood retinal barrier dysfunction

Cited by 50 publications

References 35 publications

Protective Effects of PACAP in the Retina

Protective Effects of PACAP in the Retina

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

VIP protects human retinal microvascular endothelial cells against high glucose-induced increases in TNF-α and enhances RvD1

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