June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Gap Junctions and Retinal Angiogenesis
Author Affiliations & Notes
  • Jessica Ackert
    Mt Sinai Medical Center, New York, NY
  • Tamas Atlasz
    Mt Sinai Medical Center, New York, NY
  • Footnotes
    Commercial Relationships Jessica Ackert, None; Tamas Atlasz, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 589. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Jessica Ackert, Tamas Atlasz; Gap Junctions and Retinal Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2013;54(15):589.

      Download citation file:

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

  • Supplements

Purpose: To study the role of gap junctions in the development of proliferative retinal disease.

Methods: A well-established mouse model of oxygen-induced retinopathy (OIR) was used to induce proliferative retinal disease (Smith et al 1994). Briefly, litters were exposed to hyperoxic conditions (75% oxygen) from post-natal day (PD) 7 through PD 12 causing retinal vaso-obliteration. The litters were returned to room air on PD 12. The right eye of the mouse pups received a 1 µl intravitreal injection of 500 micromolar of the global gap junctional blocker meclofenamic acid (MFA) on PD12 and 13 . The left eye served as an untreated control. The relative hypoxia of room air induces a neovascular response which is maximal at PD 17-19. The mice were sacrificed at that time point; retinas isolated, flat-mounted, and stained with the vascular endothelial marker lectin. Retinas were imaged with fluorescence and confocal microscopy and amount of vaso-obliteration and neovascularization quantified using a well-described and validated method (Stahl et al 2009).

Results: Pups treated with MFA showed a significant reversal of vaso-obliteration. Specifically, we find a 72% reduction in the area of ischemia of MFA-treated eyes compared with the contralateral non-treated retinas (n=7 pups). Similarly, there is an 78% decrease in the amount of retinal neovascularization in MFA-treated retinas compared with non-treated retinas (n=7 pups).

Conclusions: Our results indicate that gap junctions play a significant role in the development of proliferative retinopathy. While further study is needed to delineate the role of individual connexins, our data suggests that blockade of gap junctions may be a theraputic target in the treatment of retinal neovascular disease.

Keywords: 609 neovascularization • 706 retinopathy of prematurity • 700 retinal neovascularization  

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.