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XB-ART-44811
J Neurosci February 8, 2012; 32 (6): 2121-8.
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Dysmorphic photoreceptors in a P23H mutant rhodopsin model of retinitis pigmentosa are metabolically active and capable of regenerating to reverse retinal degeneration.

Lee DC , Vazquez-Chona FR , Ferrell WD , Tam BM , Jones BW , Marc RE , Moritz OL .


Abstract
This study evaluated the capacity of Xenopus laevis retina to regenerate photoreceptor cells after cyclic light-mediated acute rod photoreceptor degeneration in a transgenic P23H mutant rhodopsin model of retinits pigmentosa. After discontinuation of cyclic light exposure, we monitored histologic progression of retinal regeneration over a 3 week recovery period. To assess their metabolomic states, contralateral eyes were processed for computational molecular phenotyping. We found that retinal degeneration in the P23H rhodopsin mutation could be partially reversed, with regeneration of rod photoreceptors recovering normal morphology (including full-length rod outer segments) by the end of the 3 week recovery period. In contrast, retinal degeneration mediated by directly induced apoptosis did not recover in the 3 week recovery period. Dystrophic rod photoreceptors with truncated rod outer segments were identified as the likely source of rod photoreceptor regeneration in the P23H retinas. These dystrophic photoreceptors remain metabolically active despite having lost most of their outer segments.

PubMed ID: 22323724
PMC ID: PMC3710121
Article link: J Neurosci
Grant support: [+]

Species referenced: Xenopus laevis
Genes referenced: casp9 rho rlbp1
Antibodies: Wheat Germ Agglutinin


Article Images: [+] show captions
References [+] :
Berson, Retinitis pigmentosa. The Friedenwald Lecture. 1993, Pubmed