The neuroprotective effects of PACAP in monosodium glutamate-induced retinal lesion involve inhibition of proapoptotic signaling pathways

Rácz, Bóglárka; Gallyas, Ferenc; Kiss, P.; Tóth, Gábor; Hegyi, Orsolya; Gasz, Balázs; Borsiczky, Balázs; Ferencz, A.; Röth, Erzsébet; Tamás, Andrea; Lengvári, Istvàn; Lubics, Andrea; Reglődi, Dóra

doi:10.1016/j.regpep.2006.02.009

Cited by 66 publications

(52 citation statements)

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“…Retinal MSG excitotoxicity leads to degeneration of cells in all retinal layers through a complex mechanism involving apoptosis (23,24). The inner retinal cells bear functional ionotropic glutamate receptors, the potential targets of MSG toxicity.…”

Section: Discussionmentioning

confidence: 99%

Urocortin 2 treatment is protective in excitotoxic retinal degeneration

Szabadfi¹,

Kiss²,

Reglődi³

et al. 2014

Acta Physiologica Hungarica

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Urocortin 2 (Ucn 2) is a corticotrop releasing factor paralog peptide with many physiological functions and it has widespread distribution. There are some data on the cytoprotective effects of Ucn 2, but less is known about its neuro-and retinoprotective actions. We have previously shown that Ucn 2 is protective in ischemia-induced retinal degeneration. The aim of the present study was to examine the protective potential of Ucn 2 in monosodiumglutamate (MSG)-induced retinal degeneration by routine histology and to investigate cell-type specific effects by immunohistochemistry. Rat pups received MSG applied on postnatal days 1, 5 and 9 and Ucn 2 was injected intravitreally into one eye. Retinas were processed for histology and immunocytochemistry after 3 weeks. Immunolabeling was determined for glial fibrillary acidic protein, vesicular glutamate transporter 1, protein kinase Cα, calbindin, parvalbumin and calretinin. Retinal tissue from animals treated with MSG showed severe degeneration compared to normal retinas, but intravitreal Ucn 2 treatment resulted in a retained retinal structure both at histological and neurochemical levels: distinct inner retinal layers and rescued inner retinal cells (different types of amacrine and rod bipolar cells) could be observed. These findings support the neuroprotective function of Ucn 2 in MSG-induced retinal degeneration.

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Section: Discussionmentioning

confidence: 99%

Urocortin 2 treatment is protective in excitotoxic retinal degeneration

Szabadfi¹,

Kiss²,

Reglődi³

et al. 2014

Acta Physiologica Hungarica

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“…PACAP exerts its protective effects by increasing antiapoptotic factors and decreasing proapoptotic factors in different retinal and other injuries (Martin et al, 2004;Racz et al, 2006;Szabo et al, 2012;Vaudry et al, 2009). PACAP-induced pathways attenuate apoptosis in DR. Four pathways influenced by PACAP (MAPKs, PI3K/Akt, PKC, and inhibiting ER stress) converge to minimize apoptotic damage of retinal neurons in PACAP-treated diabetic retinas.…”

Section: P1025mentioning

confidence: 99%

“…PACAP reduces apoptosis via (iv) elevated level of p-Akt protein and its downstream target GSK3b phosphorylation. Akt signaling seems to play an important role in the neuroprotective effects of PACAP in DR (Szabadfi et al, 2014) and also other different retinal and other injuries (Lazarovici et al, 2012;Li et al, 2005;Racz et al, 2006;Szabo et al, 2012). Most of the cytoprotective effects of PACAP are mediated through activation of PAC1-R, which can induce a signaling cascade to stimulate protective factors and block caspase activation (Seaborn et al, 2011).…”

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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“…[10][11] A PACAP-38 antiapoptotikus, antiinflammatórikus és antioxidáns protektív hatása számos in vitro és in vivo kí-sérletben igazolódott. [12][13][14][15] Pontosan még nincs tisztázva, hogy milyen mechanizmusokon keresztül hat, de az igen, hogy a bélszöveti I/R-s károsodás a béltraktusban citokinfelszabadulást eredményez. 16 Számos gyulladásos modellben leírták, hogy a PACAP antiinflammatórikus hatása részben a citokinek és kemokinek termelődésének gátlása révén érvényesül.…”

Section: Bevezetésunclassified

A PACAP-38 citoprotektív és antiinflammatórikus hatásának vizsgálata vékonybél-autotranszplantációs modellben

Nedvig

Szabó

Csukás

et al. 2013

MaSeb

Self Cite

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Bevezetés: A vékonybél ischaemia-reperfusióval szembeni fokozott érzékenysége a szerv transzplantációjakor is jelen lévő probléma. Ismert a hypophysis adenilát-cikláz aktiváló polipeptid (PACAP) sejtvédő hatása. Munkánkban azt vizsgáltuk, hogy PACAP-38-at tartalmazó University of Wisconsin (UW) oldatban történő konzerválás hogyan befolyá-solja a szöveti PACAP-és citokinszinteket. Anyag és módszer: Wistar-patkányokon (n = 56) vékonybél-autotranszplantációt végeztünk. A graftokat 4 °C-os UW oldatban tároltuk 1 (I. csoport), 3 (II.) és 6 órán (III.), illetve 100 μg PACAP-38-at tartalmazó UW oldatban 1 (IV.), 3 (V.) és 6 órán (VI.) át. A reperfusio 3 óra volt. Bélmintákból a PACAP-38-és PACAP-27-szinteket radioimmunassayjel határoztuk meg, míg a citokinexpressiót kemilumineszcens módszerrel és Luminex Multiplex Immunoassayjel mértük. Eredmények: A szöveti PACAP-38-szint a kontrollhoz (57,32 ± 3,5 fmol/mg) képest a konzerválás idejével csökkent, és 6 óra után szignifikáns volt (III.: 32,6 ± 3,9 fmol/mg, p < 0,05), míg a IV-VI. csoportoknál szignifikánsan nőtt. A PACAP-27 szöveti értéke is hasonló tendenciával változott. Az sICAM-1, L-selectin és a metalloproteáz-1 szöveti inhibitorának emelkedett expressióját mértük a III. csoportban, és jelentős csökkenés volt a VI. csoportban. Következtetés: UW oldathoz adott PACAP-38 növelte a szöveti PACAP-38-és PACAP-27-szinteket, és csökkentette a citokinexpressiót. Mindez a PACAP-38 citoprotektív és anti-inflammatórikus hatását jelzi bél-autotranszplantációs modellben.Támogatta: OTKA (PD77474, 104984, CNK78480), MTA Bolyai-ösztöndíj és Lendület program. Kulcsszavak: vékonybél, transzplantáció, PACAP-38, PACAP-27, citokinexpressioIntroduction: The small intestine is one of the most sensitive organs to ischemia-reperfusion injury during transplantation. Cytoprotective effect of pituitary adenylate cyclase-activating polypeptide (PACAP) is well known. The aim of our study was to measure changes of PACAP-38-like immunoreactivities and cytokine levels in intestinal grafts stored PACAP-38 containing preservation solution. Material and methods: Small-bowel autotransplantation was performed on male Wistar rats (n = 56). Grafts were stored in University of Wisconsin (UW) solution at 4 °C for 1 (GI), 3 (GII), and 6 hours (GIII); and in PACAP-38 containing UW solution for 1 (GIV), 3 (GV), and 6 hours (GVI). Reperfusion lasted 3 hours in each group. Intestinal PACAP-38 immunoreactivities were measured by radioimmunoassay. To measure cytokine from tissue homogenates we used rat cytokine array and Luminex Multiplex Immunoassay. Results: Levels of PACAP-38-like and PACAP-27-like immunoreactivities decreased by preservation time compared to control. This decrease was significant following 6 hours cold storage (p < 0.05). Values remained significantly higher in grafts stored in PACAP-38 containing UW. Expressions of sICAM-1, L-selectin, tissue inhibitor of metalloproteinase-1 were increased in GIII and were decreased in GVI. Conclusion: PACAP-38 increased tissue levels of PACAP-38 and PACAP-27...

show abstract

The neuroprotective effects of PACAP in monosodium glutamate-induced retinal lesion involve inhibition of proapoptotic signaling pathways

Cited by 66 publications

References 50 publications

Urocortin 2 treatment is protective in excitotoxic retinal degeneration

Urocortin 2 treatment is protective in excitotoxic retinal degeneration

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

A PACAP-38 citoprotektív és antiinflammatórikus hatásának vizsgálata vékonybél-autotranszplantációs modellben

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