Endothelial Activation By Platelets From Sickle Cell Anemia Patients

dc.creatorProenca-Ferreira R.
dc.creatorBrugnerotto A.F.
dc.creatorGarrido V.T.
dc.creatorDominical V.M.
dc.creatorVital D.M.
dc.creatorRibeiro M.F.R.
dc.creatorSantos M.E.D.
dc.creatorTraina F.
dc.creatorOlalla-Saad S.T.
dc.creatorCosta F.F.
dc.creatorConran N.
dc.date2014
dc.date2015-06-25T17:55:11Z
dc.date2015-11-26T14:36:31Z
dc.date2015-06-25T17:55:11Z
dc.date2015-11-26T14:36:31Z
dc.date.accessioned2018-03-28T21:40:24Z
dc.date.available2018-03-28T21:40:24Z
dc.identifier
dc.identifierPlos One. Public Library Of Science, v. 9, n. 2, p. - , 2014.
dc.identifier19326203
dc.identifier10.1371/journal.pone.0089012
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84895809710&partnerID=40&md5=b7a9d97c01d243fd3e257ce26a03d539
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/86780
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/86780
dc.identifier2-s2.0-84895809710
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1248783
dc.descriptionSickle cell anemia (SCA) is associated with a hypercoagulable state. Increased platelet activation is reported in SCA and SCA platelets may present augmented adhesion to the vascular endothelium, potentially contributing to the vaso-occlusive process. We sought to observe the effects of platelets (PLTs) from healthy control (CON) individuals and SCA individuals on endothelial activation, in vitro. Human umbilical vein endothelial cells (HUVEC) were cultured, in the presence, or not, of washed PLTs from CON or steady-state SCA individuals. Supernatants were reserved for cytokine quantification, and endothelial adhesion molecules (EAM) were analyzed by flow cytometry; gene expressions of ICAM1 and genes of the NF-kB pathway were analyzed by qPCR. SCA PLTs were found to be more inflammatory, displaying increased adhesive properties, an increased production of IL-1β and a tendency towards elevated expressions of P-selectin and activated αIIbβ 3. Following culture in the presence of SCA PLTs, HUVEC presented significant augmentations in the expressions of the EAM, ICAM-1 and E-selectin, as well as increased IL-8 production and increased ICAM1 and NFKB1 (encodes p50 subunit of NF-κB) gene expressions. Interestingly, transwell inserts abolished the effects of SCA PLTs on EAM expression. Furthermore, an inhibitor of the NF-κB pathway, BAY 11-7082, also prevented the induction of EAM expression on the HUVEC surface by SCA PLTs. In conclusion, we find further evidence to indicate that platelets circulate in an activated state in sickle cell disease and are capable of stimulating endothelial cell activation. This effect appears to be mediated by direct contact, or even adhesion, between the platelets and endothelial cells and via NFκB-dependent signaling. As such, activated platelets in SCD may contribute to endothelial activation and, therefore, to the vaso-occlusive process. Results provide further evidence to support the use of anti-platelet approaches in association with other therapies for SCD. © 2014 Proença-Ferreira et al.
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dc.languageen
dc.publisherPublic Library of Science
dc.relationPLoS ONE
dc.rightsaberto
dc.sourceScopus
dc.titleEndothelial Activation By Platelets From Sickle Cell Anemia Patients
dc.typeArtículos de revistas


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