June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
FZD4 haploinsufficiency delays recovery of retinopathy in the ocular ischemic retinopathy (OIR) mouse model
Author Affiliations & Notes
  • Michael Hung Ngo
    Pharmacology, Dalhousie University, Halifax, NS, Canada
  • johanna borowska
    Pharmacology, Dalhousie University, Halifax, NS, Canada
  • sara nejat
    Pharmacology, Dalhousie University, Halifax, NS, Canada
  • Melanie Kelly
    Pharmacology, Dalhousie University, Halifax, NS, Canada
  • Chris McMaster
    Pharmacology, Dalhousie University, Halifax, NS, Canada
  • Johane M Robitaille
    Opthalmology, Dalhousie University, Halifax, NS, Canada
  • Footnotes
    Commercial Relationships Michael Ngo, None; johanna borowska, None; sara nejat, None; Melanie Kelly, None; Chris McMaster, None; Johane Robitaille, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 3400. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Michael Hung Ngo, johanna borowska, sara nejat, Melanie Kelly, Chris McMaster, Johane M Robitaille, ; FZD4 haploinsufficiency delays recovery of retinopathy in the ocular ischemic retinopathy (OIR) mouse model. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):3400.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: Genes in the Norrin-FZD4 signaling pathway have been implicated as risk factors for the development of severe retinopathy of prematurity (ROP). In this study, we measure the effects of FZD4 haploinsufficiency on the course of retinopathy in a Fzd4 mouse model using a modified ocular ischemic retinopathy (OIR) protocol.

Methods: The development and recovery of retinopathy in B6;129-Fzd4tm1Nat/J mice was compared to wild-type mice (C57BL/6J) at P12, P17 and P25. Retinas harvested at each time point were stained with conjugated lectin to visualize the endothelium. Flat mounted retinas were imaged, and the avascular and total areas were quantified using Image J software with the NV_Swift plugin. Vessel count and structure were quantitatively analyzed and compared in the areas that remained vascularized in the periphery and in the central area following revascularization.

Results: A significant delay in revascularization was detected at P17 in the heterozygous Fzd4 mice compared to wild-type. The delay in revascularization recovered by P25. No difference was measured in maximum vaso-obliteration at P12 or maximum neovascularization at P17. No difference in the vessel count or structure was found.

Conclusions: FZD4 haploinsufficiency causes a delay in revascularization of vaso-obliterated retina in this modified OIR mouse model. This supports previous studies demonstrating an association between rare polymorphisms/mutations in genes in this pathway and severe ROP, and suggests a possible mechanism for increasing the risk of severe ROP in humans by lengthening the period during which complications from ROP can occur.<br />

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×