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Lutein facilitates physiological revascularization in a mouse model of retinopathy of prematurity
Author(s) -
Fu Zhongjie,
Meng Steven S,
Burnim Samuel B,
Smith Lois EH,
Lo Amy CY
Publication year - 2017
Publication title -
clinical and experimental ophthalmology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.3
H-Index - 74
eISSN - 1442-9071
pISSN - 1442-6404
DOI - 10.1111/ceo.12908
Subject(s) - lutein , retinopathy of prematurity , medicine , retinal , neovascularization , ophthalmology , retina , diabetic retinopathy , macular degeneration , gliosis , ischemia , pathogenesis , retinopathy , vasculogenesis , endothelial stem cell , angiogenesis , pathology , endocrinology , biology , carotenoid , pregnancy , biochemistry , neuroscience , gestational age , genetics , diabetes mellitus , in vitro
Background Retinopathy of prematurity is one of the leading causes of childhood blindness worldwide, with vessel growth cessation and vessel loss in phase I followed by neovascularization in phase II. Ischaemia contributes to its pathogenesis, and lutein protects against ischaemia‐induced retinal damages. We aimed to investigate the effects of lutein on a murine model of oxygen‐induced retinopathy. Methods Mouse pups were exposed to 75% oxygen for 5 days and returned to room air for another 5 days. Vascular obliteration, neovascularization and blood vessel leakage were examined. Immunohistochemistry for glial cells and microglia were performed. Results Compared with vehicle controls, mouse pups receiving lutein treatment displayed smaller central vaso‐obliterated area and reduced blood vessel leakage. No significant difference in neovascular area was found between lutein and vehicle controls. Lutein promoted endothelial tip cell formation and maintained the astrocytic template in the avascular area in oxygen‐induced retinopathy. No significant changes in Müller cell gliosis and microglial activation in the central avascular area were found in lutein‐treated pups. Conclusions Our observations indicated that lutein significantly promoted normal retinal vascular regrowth in the central avascular area, possibly through promoting endothelial tip cell formation and preserving astrocytic template. Our results indicated that lutein might be considered as a supplement for the treatment of proliferative retinopathy of prematurity because of its role in facilitating the revascularization of normal vasculature.