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Acute hypoxia signals mediated by reactive oxygen species: from superoxide production to thiol modification

AuthorsHernansanz-Agustín, Pablo; Izquierdo-Álvarez, Alicia; Martínez-Ruiz, Antonio
Issue Date2014
CitationGEIRLI 2014
AbstractThe adaptation to decreased oxygen availability (hypoxia) is crucial for proper cell function and survival. In metazoans, this is partly achieved through gene transcriptional responses mediated by the hypoxia-inducible factors (HIF). There is still a debate on whether the production of reactive oxygen species (ROS) increases in hypoxia, which in turn may contribute to the activation of the HIF pathway. In addition to altering the cellular redox balance, leading to oxidative stress, ROS are capable of transducing signals by reversibly modifying the redox state of cysteine residues of proteins. We have used different techniques for measuring superoxide production kinetics, and we have observed that acute hypoxia produces a superoxide burst in different types of cells. By using diverse thiol redox proteomics techniques, we have observed an increase in cysteine reversible oxidation in endothelial cells in acute hypoxia. Indeed, we have been able to identify a number of proteins that are specifically oxidised in these conditions. These cysteine oxidation signals may mediate different adaptations to hypoxia, before the HIF pathway is fully activated. We hypothesize that ROS signals can be initiated by increased superoxide production in mitochondria, which can be translated in the oxidation of sensitive cysteine residues in cells subjected to acute hypoxia, mediating further functional adaptations.
DescriptionResumen del trabajo presentado al X Meeting of the Spanish Group for Research on Free Radicals: "Symposium on Oxidative Stress and Redox Signaling in Biology and Medicine", celebrado en la Facultad de Medicina de la Universidad de Valencia (España) del 2 al 4 de junio de 2014.-- et al.
Appears in Collections:(IIBM) Comunicaciones congresos
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