Bibliographic Details
| Title: |
Oxidative stress induces loss of pericyte coverage and vascular instability in PGC-1α-deficient mice. |
| Authors: |
García-Quintans, Nieves, Sánchez-Ramos, Cristina, Prieto, Ignacio, Tierrez, Alberto, Arza, Elvira, Alfranca, Arantzazu, Redondo, Juan, Monsalve, María |
| Source: |
Angiogenesis; Apr2016, Vol. 19 Issue 2, p217-228, 12p |
| Subject Terms: |
OXIDATIVE stress, PERICYTES, PGC-1 protein, LABORATORY mice, METABOLISM, REACTIVE oxygen species |
| Abstract: |
Peroxisome 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. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |
