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Photoreceptor glucose metabolism determines normal retinal vascular growth

Journal article
Authors Zhongjie Fu
Chatarina 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
Published in EMBO Molecular Medicine
Volume 10
Issue 1
Pages 76-90
ISSN 1757-4676
Publication year 2017
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Pages 76-90
Language en
Keywords Adiponectin, Hyperglycemia, Metabolism, Photoreceptor, Retinopathy of prematurity
Subject categories Ophthalmology


© 2017 EMBO. 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 of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth. We here examined whether hyperglycemia and low adiponectin (APN) levels delayed normal retinal vascularization, driven primarily by dysregulated photoreceptor metabolism. In premature infants, low APN levels correlated with hyperglycemia and delayed retinal vascular formation. Experimentally in a neonatal mouse model of postnatal hyperglycemia modeling early ROP, hyperglycemia caused photoreceptor dysfunction and delayed neurovascular maturation associated with changes in the APN pathway; recombinant mouse APN or APN receptor agonist AdipoRon treatment normalized vascular growth. APN deficiency decreased retinal mitochondrial metabolic enzyme levels particularly in photoreceptors, suppressed retinal vascular development, and decreased photoreceptor platelet-derived growth factor (Pdgfb). APN pathway activation reversed these effects. Blockade of mitochondrial respiration abolished AdipoRon-induced Pdgfb increase in photoreceptors. Photoreceptor knockdown of Pdgfb delayed retinal vascular formation. Stimulation of the APN pathway might prevent hyperglycemia-associated retinal abnormalities and suppress phase I ROP in premature infants.

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