title: Lutein facilitates physiological revascularization in a mouse model of retinopathy of prematurity.
abstract: 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.
authors.affiliation: Department of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.|Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Zhongjie
authors.identifier: http://orcid.org/0000-0002-8182-2983
authors.initials: Z
authors.lastname: Fu
authors.affiliation: Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Steven S
authors.initials: SS
authors.lastname: Meng
authors.affiliation: Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Samuel B
authors.initials: SB
authors.lastname: Burnim
authors.affiliation: Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Lois Eh
authors.initials: LE
authors.lastname: Smith
authors.affiliation: Department of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.|Research Center of Heart, Brain, Hormone and Healthy Aging, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong.
authors.forename: Amy Cy
authors.initials: AC
authors.lastname: Lo
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D014975:Lutein / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009389:Neovascularization, Pathologic; D009457:Neuroglia / Q000187:drug effects; D015861:Retinal Neovascularization / Q000473:pathology / Q000517:prevention & control*; D012171:Retinal Vessels / Q000187:drug effects* / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000188:drug therapy* / Q000473:pathology
chemical_list: D014975:Lutein
keywords: oxygen-induced retinopathy; retinopathy of prematurity; vascular development