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Updated: Mar 9, 2026
Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
Published on: June 23, 2014
Lutein facilitates physiological revascularization in a mouse model of retinopathy of prematurity
Zhongjie Fu1,2, Steven S Meng2, Samuel B Burnim2
1Department of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.
Insights
Lutein supplementation in oxygen-induced retinopathy models reduced blood vessel leakage and promoted normal retinal vascular regrowth. This suggests lutein may aid in treating retinopathy of prematurity by supporting vascular repair.
Area of Science:
- Ophthalmology
- Neonatal Medicine
- Retinal Vascular Biology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of childhood blindness.
- ROP involves retinal ischemia, vessel loss, and abnormal neovascularization.
- Lutein is known to protect against ischemia-induced retinal damage.
Purpose of the Study:
- To investigate the therapeutic effects of lutein on oxygen-induced retinopathy (OIR) in a murine model.
- To assess lutein's impact on retinal vascular changes in OIR.
Main Methods:
- Murine pups were exposed to hyperoxia followed by normoxia to induce retinopathy.
- Vascular obliteration, neovascularization, and blood vessel leakage were quantified.
- Immunohistochemistry was used to evaluate glial cells and microglia.
Main Results:
- Lutein treatment reduced central avascularity and blood vessel leakage.
- No significant difference in neovascularization was observed between lutein and control groups.
- Lutein promoted endothelial tip cell formation and preserved the astrocytic template.
Conclusions:
- Lutein facilitates normal retinal vascular regrowth in OIR, likely by enhancing endothelial tip cell formation and maintaining the astrocytic template.
- Lutein shows potential as a supplement for treating proliferative retinopathy of prematurity by aiding normal vascularization.
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.
