April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Short And Long-term Changes In The Retina Of A Xenopus Laevis P23H Mutant Rhodopsin Model Of Retinitis Pigmentosa
Author Affiliations & Notes
  • Damian C. Lee
    Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada
  • Beatrice M. Tam
    Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada
  • Felix R. Vazquez-Chona
    Ophthalmology, Univ of Utah, Salt Lake City, Utah
  • William D. Ferrell
    Ophthalmology, Moran Eye Center, Salt Lake City, Utah
  • Bryan W. Jones
    Ophthalmology, Moran Eye Center, Salt Lake City, Utah
  • Robert E. Marc
    Ophthalmology-Sch of Med, Univ of Utah/Moran Eye Center, Salt Lake City, Utah
  • Orson L. Moritz
    Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada
  • Footnotes
    Commercial Relationships  Damian C. Lee, None; Beatrice M. Tam, None; Felix R. Vazquez-Chona, None; William D. Ferrell, None; Bryan W. Jones, None; Robert E. Marc, Signature Immunologics (E); Orson L. Moritz, ARIAD Pharmaceuticals (F)
  • Footnotes
    Support  CIHR and FFB Canada (OLM); RPB Career Development Award, Edward N. and Della L. Thome Memorial Foundation (BWJ); NIH EY02576, NIH EY015128, NSF 0941717 and NIH EY014800 (REM).
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4337. doi:
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      Damian C. Lee, Beatrice M. Tam, Felix R. Vazquez-Chona, William D. Ferrell, Bryan W. Jones, Robert E. Marc, Orson L. Moritz; Short And Long-term Changes In The Retina Of A Xenopus Laevis P23H Mutant Rhodopsin Model Of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4337.

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

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Abstract

Purpose: : The Xenopus laevis retina can regenerate after traumatic physical injury. We wanted to determine whether the X. laevis retina is also capable of regenerating photoreceptor cells after targeted photoreceptor degeneration in a P23H mutant rhodopsin transgenic X. laevis model of retinits pigmentosa.

Methods: : We have previously developed and extensively characterized a P23H mutant rhodopsin light-inducible model of retinitis pigmentosa. In the current study, acute rod photoreceptor degeneration was induced by light exposure and documented in sample animals by histology over a 2-week period. Contralateral eyes were also processed for computational molecular phenotyping (CMP) to assess their metabolic states. The degeneration-inducing stimuli was subsequently discontinued, and retinal changes were similarly monitored over a 2-week recovery period. All procedures were performed in accordance to the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research.

Results: : Degenerating P23H photoreceptors persisted and did not immediately undergo apoptosis during the 2-week light damage period. Retinal degeneration caused by P23H rhodopsin and light damage could be partially reversed with regeneration of significant numbers of rod photoreceptors, likely from dystrophic rod photoreceptors lacking rod outer segments as the source of rod photoreceptor regeneration in the P23H retinas. Conversely, retinal degeneration caused by induction of apoptosis by direct activation of caspase 9 was permanent.

Conclusions: : Light-induced retinal degeneration mediated by P23H mutant rhodopsin is partially reversible. In this model, many rod photoreceptors are dystrophic after light exposure, but remain viable. Destabilized P23H rhodopsin protein may induce an ER stress response as a cell protective mechanism. These degenerating photoreceptors are able to re-grow lost outer segments, and partially repopulate the retina, after the degeneration-inducing stimulus is removed. However, the X. laevis retina is not capable of regenerating photoreceptors that undergo apoptotic cell death.

Keywords: retinal degenerations: cell biology • photoreceptors • cell survival 
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