Photoreceptor glucose metabolism determines normal retinal vascular growth

• DOI: 10.15252/emmm.201707966
• Publication Date: 2017-11-28T01:25:30Z
• Authors: Zhongjie Fu; Chatarina A Löfqvist; Raffael Liegl; Zhongxiao Wang; Ye Sun; Yan Gong; Chi‐Hsiu Liu; Steven S Meng; Samuel B Burnim; Ivana Arellano; My T Chouinard; Rubi Duran; Alexander Poblete; Steve S Cho; James D Akula; Michael Kinter; David Ley; Ingrid Hansen Pupp; Saswata Talukdar; Ann Hellström; Lois EH Smith
• Keywords: Carbohydrate Metabolism

The neural cells and factors determining normal vascular growth are not well defined even though vision-threatening neovessel growth, a major cause of blindness in retinopathy prematurity (ROP) (and diabetic retinopathy), is driven by delayed growth. We here examined whether hyperglycemia low adiponectin (APN) levels retinal vascularization, primarily dysregulated photoreceptor metabolism. In premature infants, APN correlated with formation. Experimentally neonatal mouse model postnatal modeling early ROP, caused dysfunction neurovascular maturation associated changes the pathway; recombinant or receptor agonist AdipoRon treatment normalized deficiency decreased mitochondrial metabolic enzyme particularly photoreceptors, suppressed development, platelet-derived factor (Pdgfb). pathway activation reversed these effects. Blockade respiration abolished AdipoRon-induced Pdgfb increase photoreceptors. Photoreceptor knockdown Stimulation might prevent hyperglycemia-associated abnormalities suppress phase I ROP infants.