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La hipoxia induce la expresion de la lisil oxidasa (LOX) en celulas endoteliales / Hypoxia induces lysyl oxidase (LOX) expression in endotelial cells
Guadall, Anna; Alcudia, Javier F; Badimon, Lina; Gentile, Maurizio; Rodriguez, Cristina; Martinez-Gonzalez, Jose.
Affiliation
  • Guadall, Anna; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
  • Alcudia, Javier F; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
  • Badimon, Lina; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
  • Gentile, Maurizio; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
  • Rodriguez, Cristina; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
  • Martinez-Gonzalez, Jose; Hospital de la Santa Creu i Sant Pau. Centro de Investigacion Cardiovascular (CSIC-ICC). Barcelona. España
Clín. investig. arterioscler. (Ed. impr.) ; 21(6): 273-280, nov.-dic. 2009. graf
Article in Es | IBECS | ID: ibc-89384
Responsible library: ES1.1
Localization: BNCS
RESUMEN
Introduccion. La hipoxia participa en el desarrollo de enfermedades cardiovasculares por la regulacion coordinada de multiples genes, incluidos aquellos implicados en la sintesis/ reparacion de la matriz extracelular (MEC). La lisil oxidasa (LOX), enzima implicada en la maduracion de la MEC, parece tener un papel clave en el mantenimiento de la homeostasis del endotelio. Nuestro objetivo fue determinar si la hipoxia modula la expresion de la LOX en celulas (..) (AU)
ABSTRACT
Introduction. Hypoxia actively participates in the pathogenesis of cardiovascular diseases through the coordinate regulation of several genes including those involved in extracellular matrix (ECM) synthesis/repair. Lysyl oxidase (LOX) is an enzyme involved in the maturation of ECM that seems to play a key role in the maintenance of endothelial homeostasis. Our aim was to determine if hypoxia could modulate endothelial LOX expression. Methods. LOX expression in bovine aortic endothelial cells (BAEC) and human umbilical cord vein endothelial cells (HUVEC) was assessed by real time PCR. LOX activity was evaluated by a fluorimetric method and LOX transcriptional activity by means of transient transfection studies. Results. Hypoxia (1% O2) increased LOX expression in both BAEC and HUVEC in conditions in which HIF-1¦Á levels, VEGF expression and neovessel formation were induced. We observed that this effect was associated to a significant increase in LOX enzymatic activity. Similarly, stimulation of endothelial cells with dimethyl-oxal-glycine, an inhibitor of prolyl hydroxylases, augmented mRNA LOX levels. Transcription inhibition with 5,6dichlorobenzimidazole prevented this effect, suggesting the involvement of a transcripcional mechanism. In agreement, transient transfection studies demonstrated that both hypoxia and HIF1¦Á over-expression induced LOX transcripcional activity to a similar extent. Conclusions. Hypoxia induces LOX expression and activity in endothelial cells through an HIF-1dependent transcriptional mechanism (AU)
Subject(s)
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Collection: 06-national / ES Database: IBECS Main subject: Cardiovascular Diseases / Cell Hypoxia / Protein-Lysine 6-Oxidase Limits: Animals / Humans Language: Es Journal: Clín. investig. arterioscler. (Ed. impr.) Year: 2009 Type: Article
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Collection: 06-national / ES Database: IBECS Main subject: Cardiovascular Diseases / Cell Hypoxia / Protein-Lysine 6-Oxidase Limits: Animals / Humans Language: Es Journal: Clín. investig. arterioscler. (Ed. impr.) Year: 2009 Type: Article