Investigative Ophthalmology & Visual Science Cover Image for Volume 61, Issue 7
June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
E-selectin is associated with the development of neovascularization in the rat model of oxygen induced retinopathy
Author Affiliations & Notes
  • Colin Andrew Bretz
    Ophthalmology, Moran Eye Center, Salt Lake City, Utah, United States
  • Eric Kunz
    Ophthalmology, Moran Eye Center, Salt Lake City, Utah, United States
  • M Elizabeth Hartnett
    Ophthalmology, Moran Eye Center, Salt Lake City, Utah, United States
  • Footnotes
    Commercial Relationships   Colin Bretz, None; Eric Kunz, None; M Elizabeth Hartnett, None
  • Footnotes
    Support  This work was supported by a career starter grant from Knights Templar Eye Foundation (CB), NIH Grants R01EY015130 and R01EY017011 (MEH), and NIH Grant EY014800 and an unrestricted grant from Research to Prevent Blindness to the Department of Ophthalmology & Visual Sciences, University of Utah.
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 5410. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Colin Andrew Bretz, Eric Kunz, M Elizabeth Hartnett; E-selectin is associated with the development of neovascularization in the rat model of oxygen induced retinopathy. Invest. Ophthalmol. Vis. Sci. 2020;61(7):5410.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose : Increased serum levels of soluble E-selectin (sE-selectin) have been associated with treatment warranted retinopathy of prematurity (ROP) in preterm infants, suggesting sE-selectin as a potential serum marker to identify preterm infants at risk of developing ROP. However, few studies have investigated the mechanistic role of E-selectin in the pathologic features found in ROP. Here we tested the hypothesis that serum levels of sE-selectin would associate with retinal E-selectin expression during the development of intravitreal neovascularization in ROP. We used an experimental model of oxygen-induced retinopathy (OIR) in the rat to test the hypothesis.

Methods : Litters of newborn rat pups were placed into an oxycycler and exposed to alternating 24hr periods of 50% and 10% oxygen for 14 days. At postnatal day (p)14, the litters were moved to room air (RA, 21% oxygen). Pups were sacrificed at p14 and p20, and serum and retinas were harvested to evaluate E-selectin expression. Serum levels of sE-selectin were measured using an ELISA assay, and retinal expression of the E-selectin gene, Sele, as well as Adam8 and Vegf, were measured using qRT-PCR. Samples from OIR treated pups were compared to those from age-matched RA-controls and analyzed using a one-way Anova.

Results : Following OIR treatment, sE-selectin was upregulated in the serum of pups at p14 (p=0.038) and p20 (p=0.028) compared to RA-controls. Retinal Sele expression, increased over time in the retinas of OIR pups and was significantly increased at p20 compared to RA-controls (p=0.031). Expression of Vegf and the metalloprotease that cleaves cell bound E-selectin, Adam8, were significantly increased in OIR pups at p14 (p=0.029 and p=0.022) and p20 (p<0.001 and p=0.032) compared to RA-controls.

Conclusions : Increased serum sE-selectin preceded the formation of intravitreal neovascularization, and both sE-selectin and retinal Sele expression were increased in association with the development of intravitreal neovascularization in the rat OIR model. sE-selectin levels were also increased in association with increased retinal Vegf and Adam8, suggesting a potential mechanism by which sE-selectin levels are increased by upregulated retinal E-selectin during the development of ROP.

This is a 2020 ARVO Annual Meeting abstract.

×
×

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.

×