Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/35238
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dc.contributor.authorNowatzki, Jenifer
dc.contributor.authorSene, Reginaldo Vieira
dc.contributor.authorPaludo, Katia Sabrina
dc.contributor.authorRizzo, Luiz Eduardo
dc.contributor.authorSouza-Fonseca-Guimaraes, Fernando
dc.contributor.authorVeiga, Silvio Sanches
dc.contributor.authorNader, Helena Bonciani [UNIFESP]
dc.contributor.authorFranco, Celia Regina C.
dc.contributor.authorTrindade, Edvaldo S.
dc.date.accessioned2016-01-24T14:27:39Z-
dc.date.available2016-01-24T14:27:39Z-
dc.date.issued2012-09-01
dc.identifierhttp://dx.doi.org/10.1016/j.toxicon.2012.04.333
dc.identifier.citationToxicon. Oxford: Pergamon-Elsevier B.V., v. 60, n. 3, p. 396-405, 2012.
dc.identifier.issn0041-0101
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/35238-
dc.description.abstractBrown spider (Loxosceles sp.) venom affects the endothelium of vessels and triggers disruptive activity in the subendothelial matrix. the vascular disorders observed after venom exposure include leukocyte and platelet activation, disseminated intravascular coagulation, an increase in vessel permeability and hemorrhage into the dermis. in this study, we report additional evidence regarding the mechanism of endothelial cell cytotoxicity induced by Loxosceles intermedia venom. Exposure to venom led to endothelial cell detachment in a time-dependent manner. Loss of cell anchorage and cell-cell adhesion following venom exposure was accompanied by changes in the distribution of the alpha(5)beta(1) integrin and VE-cadherin. An ultrastructural analysis of cells treated with venom revealed morphological alterations characteristic of apoptosis. Moreover, after venom exposure, the ratio between Bax and Bcl-2 proteins was disturbed in favor of Bax. in addition, late apoptosis was only observed in cells detached by the action of venom. Accordingly, there was no increase in apoptosis when cells were exposed to L. intermedia venom in suspension, suggesting that the loss of cell anchorage provides the signal to initiate apoptosis. Thus. L. intermedia venom likely triggers endothelial cell death indirectly through an apoptotic mechanism known as anoikis. (C) 2012 Elsevier B.V. All rights reserved.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipFundacao Araucaria-PR
dc.description.sponsorshipSecretaria de Estado de Ciencia, Tecnologia e Ensino Superior do Parana (SETI), Brazil
dc.format.extent396-405
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofToxicon
dc.rightsAcesso restrito
dc.subjectLoxosceles intermediaen
dc.subjectVenomen
dc.subjectAnoikisen
dc.subjectApoptosisen
dc.subjectEndothelial cellsen
dc.titleBrown spider (Loxosceles intermedia) venom triggers endothelial cells death by anoikisen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniv Fed Parana
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionEstadual Univ Parana
dc.description.affiliationUniv Fed Parana, Dept Cell Biol, BR-81351980 Curitiba, Parana, Brazil
dc.description.affiliationUniv Fed Parana, Dept Basic Pathol, BR-81351980 Curitiba, Parana, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biochem, BR-04044020 São Paulo, Brazil
dc.description.affiliationEstadual Univ Parana, Dept Cell Biol Mol & Genet, BR-84030900 Curitiba, Parana, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biochem, BR-04044020 São Paulo, Brazil
dc.identifier.doi10.1016/j.toxicon.2012.04.333
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000306869300020
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