title: Norrie gene product is necessary for regression of hyaloid vessels.
abstract: OBJECTIVE
  To investigate the nature and origin of the vitreous membranes in mice with knock-out of the Norrie gene product (ND mice).
  
  
  METHODS
  Eighty-two eyes of ND mice of different age groups (postnatal day [P]0-13 months) and 95 age-matched wild-type control mice were investigated. In vitreoretinal wholemounts and in sagittal sections, vessels and free cells were visualized by labeling for lectin. In addition, staining with a marker for macrophages (F4/80) and collagen XVIII/endostatin known to be involved in regression of hyaloid vessels was performed for light and electron microscopic investigations. Endostatin expression was confirmed by Western blot analysis.
  
  
  RESULTS
  Wild-type controls showed the typical pattern of hyaloid vessels, their regression and concomitantly retinal vasculogenesis and angiogenesis. Hyaloid vessels all stained for endostatin, whereas retinal vessels remained unstained. In ND mice, 1 to 5 days after birth, the hyaloid and retinal vasculatures were comparable to that in control mice. The hyaloid vessels also stained for endostatin. Numerous F4/80-positive cells were present adjacent to the vessels. With increasing age, only a few connecting branches of the hyaloid vessels regressed. Even in old mice most of the hyaloid vessels persisted. The vessels still stained for endostatin. Retinal angiogenesis was impaired.
  
  
  CONCLUSIONS
  Retrolental membranes in ND mice consist of persistent hyaloid vessels, indicating that the ND gene product is important for the process of regression of these vessels. The ND gene product neither influences endostatin expression nor the presence of macrophages.
authors.affiliation: Department of Anatomy II, Friedrich-Alexander-University, Erlangen, Germany.
authors.forename: Anne V
authors.initials: AV
authors.lastname: Ohlmann
authors.forename: Edith
authors.initials: E
authors.lastname: Adamek
authors.forename: Andreas
authors.initials: A
authors.lastname: Ohlmann
authors.forename: Elke
authors.initials: E
authors.lastname: Lütjen-Drecoll
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D001766:Blindness / Q000235:genetics; D015153:Blotting, Western; D043169:Endostatins / Q000378:metabolism; D005124:Eye Abnormalities / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D005136:Eye Proteins / Q000502:physiology*; D040181:Genetic Diseases, X-Linked / Q000235:genetics; D008566:Membranes / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D016253:Microscopy, Immunoelectron; D009419:Nerve Tissue Proteins / Q000502:physiology*; D012162:Retinal Degeneration / Q000235:genetics; D015861:Retinal Neovascularization / Q000378:metabolism / Q000473:pathology*; D012171:Retinal Vessels / Q000378:metabolism / Q000473:pathology*; D014822:Vitreous Body / Q000002:abnormalities* / Q000098:blood supply*
chemical_list: D000943:Antigens, Differentiation; D043169:Endostatins; D005136:Eye Proteins; C489916:Ndph protein, mouse; D009419:Nerve Tissue Proteins; C036763:monocyte-macrophage differentiation antigen