April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Molecular and Cellular Events Leading to Photoreceptor Cell Death in Retinitis Pigmentosa
Author Affiliations & Notes
  • Alberto M. Hernandez-Pinto
    3D Lab (Development, Differentiation & Degeneration), Cellular and Molecular Medicine, Ctr de Invest Biologicas-CSIC, Madrid, Spain
  • Natalia Rodriguez-Muela
    3D Lab (Development, Differentiation & Degeneration), Cellular and Molecular Medicine, Ctr de Invest Biologicas-CSIC, Madrid, Spain
  • Patricia Boya
    3D Lab (Development, Differentiation & Degeneration), Cellular and Molecular Medicine, Ctr de Invest Biologicas-CSIC, Madrid, Spain
  • Enrique J. de la Rosa
    3D Lab (Development, Differentiation & Degeneration), Cellular and Molecular Medicine, Ctr de Invest Biologicas-CSIC, Madrid, Spain
  • Footnotes
    Commercial Relationships  Alberto M. Hernandez-Pinto, None; Natalia Rodriguez-Muela, None; Patricia Boya, None; Enrique J. de la Rosa, None
  • Footnotes
    Support  Spanish Ministerio de Ciencia e Innovación Grants SAF2007-66175 and SAF2009-08086
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5413. doi:https://doi.org/
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      Alberto M. Hernandez-Pinto, Natalia Rodriguez-Muela, Patricia Boya, Enrique J. de la Rosa; Molecular and Cellular Events Leading to Photoreceptor Cell Death in Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5413. doi: https://doi.org/.

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

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Abstract

Purpose: : Retinitis Pigmentosa (RP) is a general term for a heterogeneous group of hereditary retinal dystrophies characterized by progressive loss of vision due to the death of photoreceptors. Although several molecular mechanisms underlying photoreceptor cell death have been characterized, the hierarchy among them is far from being understood. The aim of the present work is to establish the sequence of molecular and cellular events taking place in the photoreceptors undergoing degeneration.

Methods: : We have analyzed the sequence of events leading to cell death in the cone-derived 661W cells and in C57Bl/6 wild type retinas cultured in the presence of Zaprinast (a PDE6 inhibitor) and A23187 (a calcium ionophore), as well as in the rd10 mouse model of RP. We have determined calcium influx, oxidative stress, calpain activation, and apoptosis by flow cytometry, confocal microscopy and several enzymatic assays.

Results: : The rd10 mouse retinas showed an early increase in calcium content and calpain activation followed by an imbalance in the antioxidant defense system, with increased superoxide and oxygen peroxide production when compared to wild type retinas. A23187 and zaprinast treatments mimicked most of these alterations in the experimental models of RP.

Conclusions: : The combination of genetic and experimental models of RP provides new cues to establish the hierarchy of events leading to retinal degeneration and may assist to define new and better targets for a therapeutical intervention.

Keywords: retinitis • retinal degenerations: cell biology • calcium 
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