April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Caspase-12 Play a Role in Light-Induced Retinal Degeneration
Author Affiliations & Notes
  • M. Doly
    Biophysique des handicaps Sensoriels, School of Medicine, Clermont Ferrand, France
    Laboratoire de Biochimie, biologie Moleculaire et Nutrition, Faculte de Pharmacie, Clermont-Ferrand, France, France
  • O. Perche
    Laboratoire de Biochimie, biologie Moleculaire et Nutrition, Faculte de Pharmacie, Clermont-Ferrand, France, France
  • C. Cercy
    Biophysique des handicaps Sensoriels, School of Medicine, Clermont Ferrand, France
  • I. Ranchon-Cole
    Biophysique des handicaps Sensoriels, School of Medicine, Clermont Ferrand, France
  • Footnotes
    Commercial Relationships  M. Doly, None; O. Perche, None; C. Cercy, None; I. Ranchon-Cole, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 4485. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M. Doly, O. Perche, C. Cercy, I. Ranchon-Cole; Caspase-12 Play a Role in Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4485.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : To study caspase-12 in light-induced retinal degeneration

Methods: : Wistar rats were raised in dim-cyclic light. In a first set of experiments, rats were uninjected or injected with DMSO 2% or the caspase-12 inhibitor Z-ATAD-FMK (0,4 mM). They were placed in the dark before being exposed for 24 hours to 2700 or 3400 lux-light. They were sacrificed at 0, 2 or 24 hours of light-exposure to measure caspase-12 activity in the retina. In a second set of experiments, rats were uninjected or injected with DMSO 2% or Z-ATAD-FMK before being exposed for 24 hours to 2700 or 3400 lux light. Electroretinograms were recorded before exposure and/or treatment, at 1 day (D1) and 15 days (D15) after light-exposure to calculate Bmax (maximal b-wave amplitude). After the last ERG, rats were sacrificed and the outer nuclear layer thickness measured. Unexposed animals were processed in parallel.

Results: : Caspase-12 activity from untreated retina at 0h was set as 100%. At 0h, DMSO has no effect but Z-ATAD-FMK reduced caspase-12 activity to 52 %. At 2h of light exposure caspase-12 activity was reduced to 62 % in untreated and to 52 % in Z-ATAD-FMK retinas while it increased to 154 % in DMSO ones. At 24h, caspase-12 activity was back to the basal level in all groups. In unexposed rats, DMSO and Z-ATAD-FMK have no effect on retinal function or structure. In untreated retinas exposed to 2700 lux, the ONL in the superior part of the retina was reduced by 32% and Bmax by 33 %. DMSO was not different from untreated. Z-ATAD-FMK retinas were more preserved than DMSO. In untreated retinas exposed to 3400 lux, ONL in the superior part of the retina was reduced by 62% and Bmax by 52%. DMSO or Z-ATAD-FMK groups were not significantly different from untreated one.

Conclusions: : We have shown that the caspase-12 inhibitor Z-ATAD-FMK reaches the retina and inhibits caspase-12 activity at least at the beginning of light exposure. In these conditions, caspase-12 inhibition can protect the retina from weak light-stress Further experiments are on course to determine if an increase in caspase-12 inhibition increase its neuroprotective effect.

Keywords: apoptosis/cell death • enzymes/enzyme inhibitors • 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.

×