April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Cellular Mechanisms Controlling the Mosaic of Surviving Cones in the S334ter-line-3-rat Model of Retinitis Pigmentosa
Author Affiliations & Notes
  • Yerina Ji
    Neuroscience Graduate Program, University of Southern California, Los Angeles, California
  • Eun-Jin Lee
    Department of Biomedical Engineering, Univ of Southern California, Los Angeles, California
    Center for Vision Science and Technology, University of Southern California, Los Angeles, California
  • Colleen Zhu
    Department of Biomedical Engineering, Univ of Southern California, Los Angeles, California
  • Norberto M. Grzywacz
    Neuroscience Graduate Program, University of Southern California, Los Angeles, California
    Department of Biomedical Engineering, Univ of Southern California, Los Angeles, California
  • Footnotes
    Commercial Relationships  Yerina Ji, None; Eun-Jin Lee, None; Colleen Zhu, None; Norberto M. Grzywacz, None
  • Footnotes
    Support  NEI Grants EY11170 and EY016093, NSF Grant EEC0310723, Fight for Sight Grant
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4993. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Yerina Ji, Eun-Jin Lee, Colleen Zhu, Norberto M. Grzywacz; Cellular Mechanisms Controlling the Mosaic of Surviving Cones in the S334ter-line-3-rat Model of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4993.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : In the S334ter-line-3 rat (a transgenic model developed to express a rhodopsin mutation causing retinitis pigmentosa - RP), the rod’s death triggers a reorganization of the cone mosaic. Cones migrate into an orderly array of rings. This study was conducted to understand the cellular mechanisms controlling the resulting mosaic of surviving cones.

Methods: : S334ter-line-3 rats were used as a model of RP with control animals being age-matched Sprague Dawley rats. All rats were kept under daily 12 h light/dark cycle. Intravitreal injections into the rats’ eyes were performed with either saline, AAA (disrupting Müller-cell processes), TIMP-1 (disrupting metalloproteinases), or with mixtures of AAA and TIMP-1. Three days after the injection, the rats were sacrificed and the retinas were tested for the organization of cones and Müller-cells by immunohistochemistry. Tests of cone survival were performed with Western-blot analysis.

Results: : We observed remodeling of Müller-cell processes in RP retinas; the processes were surrounding cones and filling the space inside their rings. In contrast, no ring of cones appeared in RP retinas collected from AAA-injected eyes. In turn, RP retinas from TIMP-1-injected eyes showed rings of clusters of cones, while TIMP-1 injection in normal eyes elicited formation of spatially random clusters of cones. Mixtures of AAA and TIMP-1 eliminated the rings of cones, causing salt-and-pepper distributions of these cells. Western-blot results showed reduction in the protein levels related to cones in the absence of rings but not otherwise.

Conclusions: : At least two mechanisms may control the mosaic of surviving cones in S334ter-line-3 rats. Our results showed that Müller cells interact closely with cones, helping form ring mosaics in RP. Furthermore, the release of metalloproteinases from the retinal pigment epithelium may aid in the even spatial distribution of cones both normally and in rings. Ring formations may help to prolong the survival of cones.

Keywords: retinitis • retinal degenerations: cell biology • retina 
×
×

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.

×