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Type: Artigo de periódico
Title: Human Neutrophil Migration In Vitro Induced By Secretory Phospholipases A2: A Role For Cell Surface Glycosaminoglycans
Author: Gambero A.
Landucci E.C.T.
Toyama M.H.
Marangoni S.
Giglio J.R.
Nader H.B.
Dietrich C.P.
De Nucci G.
Antunes E.
Abstract: The purpose of this study was to examine the ability of type I- (porcine pancreas and Naja mocambique mocambique venom), type II- (bothropstoxin-I, bothropstoxin-II, and piratoxin-I), and type III- (Apis mellifera venom) secretory phospholipases A2 (sPLA2s) to induce human neutrophil chemotaxis, and the role of the cell surface proteoglycans, leukotriene B4 (LTB4), and platelet-activating factor (PAF), in mediating this migration. The neutrophil chemotaxis assays were performed by using a 48-well microchemotaxis chamber. Piratoxin-I, bothropstoxin-I, N. m. mocambique venom PLA2 (10-1000 μg/mL each), bothropstoxin-II (30-1000 μg/mL), porcine pancreas PLA2 (0.3-30 μg/mL), and A. mellifera venom PLA2 (30-300 μg/mL) caused concentration-dependent neutrophil chemotaxis. Heparin (10-300 U/mL) concentration-dependently inhibited the neutrophil migration induced by piratoxin-I, bothropstoxin-II, and N. m. mocambique and A. mellifera venom PLA2s (100 μg/mL each), but failed to affect the migration induced by porcine pancreas PLA2. Heparan sulfate (300 and 1000 μg/mL) inhibited neutrophil migration induced by piratoxin-I, whereas dermatan sulfate and chondroitin sulfate (30-1000 μg/mL each) had no effect. Heparitinase I and heparinase (300 mU/mL each) inhibited by 41.5 and 47%, respectively, piratoxin-I-induced chemotaxis, whereas heparitinase II and chondroitinase AC failed to affect the chemotaxis. The PAF receptor antagonist WEB 2086 (3-[4-(2-chlorophenyl)-9-methyl-6H-thienol-[3,2-f] [1,2,4]-triazolo-[4,3-a] [1,4]-diazepine-2-yl]-1-(4-morpholynil)-1-propionate) (0.1-10 μM) and the LTB4 synthesis inhibitor AA-861 [2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-1,4-benzoquinone] (0.1-10 μM) significantly inhibited the piratoxin-I-induced chemotaxis. Piratoxin-I (30-300 μg/mL) caused a concentration-dependent release of LTB4. Our results suggest that neutrophil migration in response to sPLA2s is independent of PLA activity, and involves an interaction of sPLA2s with cell surface heparin/heparan binding sites triggering the release of LTB4 and PAF. © 2002 Elsevier Science Inc. All rights reserved.
Rights: fechado
Identifier DOI: 10.1016/S0006-2952(01)00841-3
Date Issue: 2002
Appears in Collections:Unicamp - Artigos e Outros Documentos

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