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dc.rights.licensehttp://creativecommons.org/licenses/by-nc-sa/3.0/ve/
dc.contributor.authorVielma, Silvanaes_VE
dc.contributor.authorLopes Virella, Maria F.es_VE
dc.contributor.authorKrings, Gregores_VE
dc.date2005-07-25es_VE
dc.date.accessioned2005-07-25T09:00:00Z
dc.date.available2005-07-25T09:00:00Z
dc.date.created2005-07-25es_VE
dc.date.issued2005-07-25T09:00:00Zes_VE
dc.identifier.otherT016300002213/0es_VE
dc.identifier.urihttp://www.saber.ula.ve/handle/123456789/16107
dc.description.abstractChlamydophila pneumoniae induces ICAM-1 expression in human aortic endothelial cells via protein kinase c-dependent activation of nuclear factor-kb. (Vielma, Silvana; Krings, Gregor; Lopes Virella, Maria F.) Abstract Chlamydophila pneumoniae has an epidemiological link with atherosclerosis and acute cardiovascular events. One mechanism that may explain such a link is the increased expression of intracellular adhesion molecule-1 (ICAM-1) in C pneumoniae-infected endothelial cells. Upregulation of ICAM-1 by C pneumoniae is well recognized and has been extensively studied, but the signaling pathways involved are not yet defined. Because upregulation of ICAM-1 by cytokines and other stimuli has been shown to be mediated by either mitogen-activated protein kinase, protein kinase C (PKC), or nuclear factor-kB (NF-kB) pathways, we examined whether these pathways were involved in the ICAM-1 upregulation induced by C pneumoniae. Our data show a time-dependent phosphorylation of p44/p42 and SAPK/JNK pathways in C pneumoniae-infected cells. However, inhibition of the classic mitogen-activated protein kinase pathway using the PD98059 and U0126 inhibitors and inhibition of SAPK/JNK pathway did not suppress C pneumoniae-induced ICAM-1 expression. C pneumoniae also activates the NF-kB pathway at 30 minutes after infection. Treatment of human aortic endothelial cells (HAECs) with the NF-kB inhibitors BAY117085 and caffeic acid phenethyl ester led to a concentration-dependent inhibition of C pneumoniae-induced ICAM-1 upregulation. Finally, C pneumoniae-infected HAECs show membrane translocation of total PKC 30 minutes after cell infection. Calphostin C, a general PKC inhibitor, blocked both C pneumoniae-induced ICAM-1 expression and C pneumoniae-induced NF-kB translocation. In conclusion, we demonstrated that C pneumoniae-induced ICAM-1 expression in HAECs requires NF-kB and PKC activation and that NF-kB activation is PKC dependent.es_VE
dc.language.isoeses_VE
dc.publisherSABER ULAes_VE
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleChlamydophila pneumoniae induces ICAM-1 expression in human aortic endothelial cells via protein kinase c-dependent activation of nuclear factor-kb.es_VE
dc.typeinfo:eu-repo/semantics/article
dc.description.emailvielmasa@musc.edues_VE
dc.description.tiponivelNivel monográficoes_VE
dc.subject.departamentoDepartamento de Microbiología y Parasitologíaes_VE
dc.subject.escuelaEscuela de Medicinaes_VE
dc.subject.facultadFacultad de Medicinaes_VE
dc.subject.keywordsChlamydophila pneumoniaees_VE
dc.subject.keywordsIntercellular adhesion molecule-1es_VE
dc.subject.keywordsNuclear factor-kBes_VE
dc.subject.keywordsProtein kinase Ces_VE
dc.subject.keywordsMitogen-activated protein kinase pathwayes_VE
dc.subject.laboratorioLaboratorio de Microbiología y Salud Pública del Estado Mérida. ULA-ULEes_VE
dc.subject.tipoArtículoses_VE


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