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dc.creatorGutiérrez, José María
dc.creatorRucavado Romero, Alexandra
dc.creatorEscalante Muñoz, Teresa
dc.creatorDíaz Oreiro, Cecilia
dc.date.accessioned2017-02-24T19:50:50Z
dc.date.available2017-02-24T19:50:50Z
dc.date.issued2005-06-15
dc.identifier.citationhttp://www.sciencedirect.com/science/article/pii/S0041010105000668es_ES
dc.identifier.issn0041-0101
dc.identifier.urihttp://hdl.handle.net/10669/29553
dc.description.abstractZinc-dependent metalloproteinases are responsible for the hemorrhagic activity characteristic of viperid snake venoms. Snake venom metalloproteinases (SVMPs) are classified in various groups (P-I–IV), according to their domain composition. P-III SVMPs, comprising metalloproteinase, disintegrin-like and cysteine-rich domains, exert more potent hemorrhagic activity than P-I SVMPs, which present only the metalloproteinase domain. SVMPs degrade various components of the basement membrane and are also able to hydrolyze endothelial cell membrane proteins, such as integrins and cadherins, involved in cell–matrix and cell–cell adhesion. In addition, disintegrin-like and cysteine-rich domains interact with endothelial cell integrins, interfering with their adhesion to extracellular matrix. Hemorrhage induced by SVMPs is an extremely rapid event in vivo, with capillary endothelial cells showing drastic structural alterations within few minutes. In contrast, observations in cell culture conditions do not evidence such rapid endothelial cell damage. Instead, the main effect is detachment and rounding of these cells; it is only after several hours of incubation that cells show evidence of apoptotic damage. This apparent discrepancy between in vivo and in vitro observations can be explained if biophysical forces operating on microvessels in vivo are taken into consideration. It is proposed that SVMP-induced hemorrhage occurs in vivo by a ‘two-step’ mechanism. Initially, SVMPs degrade basement membrane and adhesion proteins, thus weakening the capillary wall and perturbing the interactions between endothelial cells and the basement membrane. Then, transmural pressure acting on the weakened capillary wall causes distention. As a consequence, endothelial cells become very thin, until the integrity of the capillary wall is lost at some points, where extravasation occurs. In addition, endothelial cells become more susceptible to blood flow-dependent shear stress, which further contributes to capillary wall disruption.es_ES
dc.description.sponsorshipUniversidad de Costa Rica//UCR/Cota Ricaes_ES
dc.description.sponsorshipConsejo Nacional para Investigaciones Científicas y Tecnológicas//CONICIT/Costa Ricaes_ES
dc.description.sponsorshipInternational Foundation for Science//IFS/Sueciaes_ES
dc.description.sponsorshipWellcome Trust///Inglaterraes_ES
dc.description.sponsorship//AID/es_ES
dc.language.isoen_USes_ES
dc.sourceToxicon; Volumen 45, Número 8, 2005es_ES
dc.subjectSnake Venom Metalloproteinaseses_ES
dc.subjectHemorrhagees_ES
dc.subjectHemostasises_ES
dc.subjectShear Stresses_ES
dc.subjectEndothelial Cellses_ES
dc.subjectApoptosises_ES
dc.subjectSnake venomes_ES
dc.titleHemorrhage induced by snake venom metalloproteinases: biochemical and biophysical mechanisms involved in microvessel damagees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.typeArtículo científicoes_ES
dc.identifier.doi10.1016/j.toxicon.2005.02.029
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP)es_ES
dc.identifier.pmid15922771


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