Peptide gomesin triggers cell death through L-type channel calcium influx, MAPK/ERK, PKC and PI3K signaling and generation of reactive oxygen species

Show simple item record Soletti, Rossana C. del Barrio, Laura Daffre, Sirlei Miranda, Antonio [UNIFESP] Borges, Helena L. Moura-Neto, Vivaldo Lopez, Manuela G. Gabilan, Nelson H. 2016-01-24T14:05:13Z 2016-01-24T14:05:13Z 2010-07-30
dc.identifier.citation Chemico-biological Interactions. Clare: Elsevier B.V., v. 186, n. 2, p. 135-143, 2010.
dc.identifier.issn 0009-2797
dc.description.abstract Gomesin is an antimicrobial peptide isolated from hemocytes of a common Brazilian tarantula spider named Acanthoscurriagomesiana. This peptide exerts antitumor activity in vitro and in vivo by an unknown mechanism. in this study, the cytotoxic mechanism of gomesin in human neuroblastoma SH-SY5Y and rat pheochromocytoma PC12 cells was investigated. Gomesin induced necrotic cell death and was cytotoxic to SH-SY5Y and PC12 cells. the peptide evoked a rapid and transient elevation of intracellular calcium levels in Fluo-4-AM loaded PC12 cells, which was inhibited by nimodipine, an L-type calcium channel blocker. Preincubation with nimodipine also inhibited cell death induced by gomesin in SH-SY5Y and PC12 cells. Gomesin-induced cell death was prevented by the pretreatment with MAPK/ERK, PKC or PI3K inhibitors, but not with PKA inhibitor. in addition, gomesin generated reactive oxygen species (ROS) in SH-SY5Y cells, which were blocked with nimodipine and MAPK/ERK, PKC or PI3K inhibitors. Taken together, these results suggest that gomesin could be a useful anticancer agent, which mechanism of cytotoxicity implicates calcium entry through L-type calcium channels, activation of MAPK/ERK, PKC and PI3K signaling as well as the generation of reactive oxygen species. (C) 2010 Elsevier Ireland Ltd. All rights reserved. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship FINEP
dc.description.sponsorship Spanish Agencies
dc.description.sponsorship Ministerio de Educacion y Ciencia
dc.description.sponsorship Fundacion Carolina, Universidad Autonoma de Madrid
dc.description.sponsorship Fundacion Teofilo Hernando
dc.format.extent 135-143
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Chemico-biological Interactions
dc.rights Acesso restrito
dc.subject Gomesin en
dc.subject Antimicrobial peptides en
dc.subject Cytotoxicity en
dc.subject Calcium channels en
dc.subject Cell signaling en
dc.subject Necrosis en
dc.title Peptide gomesin triggers cell death through L-type channel calcium influx, MAPK/ERK, PKC and PI3K signaling and generation of reactive oxygen species en
dc.type Artigo
dc.contributor.institution Univ Autonoma Madrid
dc.contributor.institution Universidade Federal de Santa Catarina (UFSC)
dc.contributor.institution Universidade Federal do Rio de Janeiro (UFRJ)
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Autonoma Madrid, Fac Med, Dept Farmacol, Inst Teofilo Hernando, E-28029 Madrid, Spain
dc.description.affiliation Univ Fed Santa Catarina, CCB, Dept Bioquim, BR-88090900 Florianopolis, SC, Brazil
dc.description.affiliation Univ Fed Rio de Janeiro, Inst Ciencias Biomed, Rio de Janeiro, Brazil
dc.description.affiliation Univ São Paulo, ICB, Dept Parasitol, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biofis, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biofis, São Paulo, Brazil
dc.description.sponsorshipID CAPES: 0013/01-3
dc.description.sponsorshipID CAPES: 173/2008
dc.description.sponsorshipID FINEP: 01.06.0842-00
dc.description.sponsorshipID Ministerio de Educacion y Ciencia: SAF2006-08540
dc.description.sponsorshipID Ministerio de Educacion y Ciencia: PHB2007-0004-PC
dc.identifier.doi 10.1016/j.cbi.2010.04.012
dc.description.source Web of Science
dc.identifier.wos WOS:000279644900005


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