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Oxidative stress induces loss of pericyte coverage and vascular instability in PGC-1α-deficient mice

AutorGarcía-Quintans, Nieves ; Sánchez-Ramos, Cristina; Prieto, Ignacio; Tierrez, Albert; Arza, Elvira; Alfranca, Arántzazu; Redondo, Juan Miguel ; Monsalve, María
Palabras claveVascular stability
ROS
Angiogenesis
Retinopathy
PGC-1α
Fecha de publicación2016
EditorSpringer
CitaciónAngiogenesis 19(2): 217-228 (2016)
ResumenPeroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) is a regulator of mitochondrial oxidative metabolism and reactive oxygen species (ROS) homeostasis that is known to be inactivated in diabetic subjects. This study aimed to investigate the contribution of PGC-1α inactivation to the development of oxygen-induced retinopathy. We analyzed retinal vascular development in PGC-1α mice. Retinal vasculature of PGC-1α mice showed reduced pericyte coverage, a de-structured vascular plexus, and low perfusion. Exposure of PGC-1α mice to hyperoxia during retinal vascular development exacerbated these vascular abnormalities, with extensive retinal hemorrhaging and highly unstructured areas as compared with wild-type mice. Structural analysis demonstrated a reduction in membrane-bound VE-cadherin, which was suggestive of defective intercellular junctions. Interestingly, PGC-1α retinas showed a constitutive activation of the VEGF-A signaling pathway. This phenotype could be partially reversed by antioxidant administration, indicating that elevated production of ROS in the absence of PGC-1α could be a relevant factor in the alteration of the VEGF-A signaling pathway. Collectively, our findings suggest that PGC-1α control of ROS homeostasis plays an important role in the regulation of de novo angiogenesis and is required for vascular stability.
Versión del editorhttps://doi.org/10.1007/s10456-016-9502-0
URIhttp://hdl.handle.net/10261/150943
DOI10.1007/s10456-016-9502-0
Identificadoresdoi: 10.1007/s10456-016-9502-0
e-issn: 1573-7209
issn: 0969-6970
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