The blockade of cyclooxygenases-1 and-2 reduces the effects of hypoxia on endothelial cells

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dc.contributor.authorGloria, Maria Aparecida da [UNIFESP]
dc.contributor.authorCenedeze, Marcos Antonio [UNIFESP]
dc.contributor.authorPacheco-Silva, Alvaro [UNIFESP]
dc.contributor.authorCamara, Niels Olsen Saraiva [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2016-01-24T12:41:25Z
dc.date.available2016-01-24T12:41:25Z
dc.date.issued2006-09-01
dc.description.abstractHypoxia activates endothelial cells by the action of reactive oxygen species generated in part by cyclooxygenases (COX) production enhancing leukocyte transmigration. We investigated the effect of specific COX inhibition on the function of endothelial cells exposed to hypoxia. Mouse immortalized endothelial cells were subjected to 30 min of oxygen deprivation by gas exchange. Acridine orange/ ethidium bromide dyes and lactate dehydrogenase activity were used to monitor cell viability. the mRNA of COX-1 and -2 was amplified and semi-quantified before and after hypoxia in cells treated or not with indomethacin, a non-selective COX inhibitor. Expression of RANTES ( regulated upon activation, normal T cell expressed and secreted) protein and the protective role of heme oxygenase-1 (HO-1) were also investigated by PCR. Gas exchange decreased partial oxygen pressure (PaO2) by 45.12 +/- 5.85% (from 162 +/- 10 to 73 +/- 7.4 mmIIg). Thirty minutes of hypoxia decreased cell viability and enhanced lactate dehydrogenase levels compared to control (73.1 +/- 2.7 vs 91.2 +/- 0.9%, P < 0.02; 35.96 +/- 11.64 vs 22.19 +/- 9.65%, P = 0.002, respectively). COX-2 and HO-1 mRNA were up-regulated after hypoxia. Indomethacin (300 mu M) decreased COX-2, HO-1, hypoxiainducible factor-1 alpha and RANTES mRNA and increased cell viability after hypoxia. We conclude that blockade of COX up-regulation can ameliorate endothelial injury, resulting in reduced production of chemokines.en
dc.description.affiliationUNIFESP, Div Nefrol, Lab Imunol Clin & Expt, Hosp Rim & Hipertensao,Fundacao Oswaldo Ramos, São Paulo, SP, Brazil
dc.description.affiliationUniv São Paulo, Dept Imunol, Inst Ciencias Biomed 4, Lab Imunobiol Transplantes, São Paulo, SP, Brazil
dc.description.affiliationUnifespUNIFESP, Div Nefrol, Lab Imunol Clin & Expt, Hosp Rim & Hipertensao,Fundacao Oswaldo Ramos, São Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.format.extent1189-1196
dc.identifierhttp://dx.doi.org/10.1590/S0100-879X2006000900006
dc.identifier.citationBrazilian Journal of Medical and Biological Research. São Paulo: Assoc Bras Divulg Cientifica, v. 39, n. 9, p. 1189-1196, 2006.
dc.identifier.doi10.1590/S0100-879X2006000900006
dc.identifier.issn0100-879X
dc.identifier.scieloS0100-879X2006000900006
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29119
dc.identifier.wosWOS:000240545900006
dc.language.isoeng
dc.publisherAssoc Bras Divulg Cientifica
dc.relation.ispartofBrazilian Journal of Medical and Biological Research
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectendothelial cellen
dc.subjecthypoxiaen
dc.subjectindomethacinen
dc.subjectcyclooxygenaseen
dc.subjectheme oxygenase 1en
dc.titleThe blockade of cyclooxygenases-1 and-2 reduces the effects of hypoxia on endothelial cellsen
dc.typeinfo:eu-repo/semantics/article
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