Structural and functional protection of photoreceptors from MNU-induced retinal degeneration by the X-linked inhibitor of apoptosis

Invest Ophthalmol Vis Sci. 2003 Jun;44(6):2757-63. doi: 10.1167/iovs.02-0729.

Abstract

Purpose: To evaluate the neuroprotective effects of adenoassociated virus delivery of XIAP in N-methyl-N-nitrosourea (MNU)-induced retinal degeneration in Sprague-Dawley rats.

Methods: Sprague-Dawley rats were injected subretinally with recombinant adenoassociated virus (rAAV) encoding either XIAP or green fluorescent protein (GFP; injection control). Six weeks after injection, the animals received an intraperitoneal injection of MNU, a DNA methylating agent, at a dose of 60 mg/kg. Electroretinograms (ERGs) were recorded at 0, 24, 48 and 72 hours and 1 week after MNU. The rats were killed after the ERG was performed and were perfused with 4% paraformaldehyde. Eyes were then enucleated and embedded for cryosectioning. Eye sections were analyzed by TUNEL and histologic techniques. Real-time PCR and Western analysis were performed to confirm the overexpression of XIAP in injected eyes.

Results: Real-time PCR and Western analysis confirmed the overexpression of XIAP in virus-injected eyes in comparison to uninjected control eyes. At 24 hours after MNU injection, fewer cells had undergone apoptosis in the XIAP-treated eyes in comparison with GFP-injected or uninjected eyes. Hematoxylin and eosin staining revealed that the uninjected and GFP-injected photoreceptors were destroyed by 72 hours after injection of MNU, whereas the AAV-XIAP-injected eyes showed structural protection of the photoreceptors at all time points throughout the 1-week sampling period. ERGs showed functional protection up to 1 week after MNU injection in the AAV-XIAP-injected eye, whereas no response was observed in the control eye.

Conclusions: The results suggest that XIAP is protective against this potent chemotoxic agent and holds promise as a therapeutic agent in gene therapy approaches to treating retinitis pigmentosa.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkylating Agents / toxicity
  • Animals
  • Apoptosis / drug effects*
  • Blotting, Western
  • Cytoprotection
  • Dependovirus / genetics
  • Electroretinography
  • Enzyme Inhibitors
  • Genetic Therapy*
  • Genetic Vectors
  • Green Fluorescent Proteins
  • In Situ Nick-End Labeling
  • Luminescent Proteins / genetics
  • Male
  • Methylnitrosourea / toxicity
  • Photoreceptor Cells, Vertebrate / cytology*
  • Photoreceptor Cells, Vertebrate / physiology*
  • Proteins / genetics*
  • Proteins / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Retinal Degeneration / chemically induced
  • Retinal Degeneration / metabolism
  • Retinal Degeneration / prevention & control*
  • Reverse Transcriptase Polymerase Chain Reaction
  • X-Linked Inhibitor of Apoptosis Protein

Substances

  • Alkylating Agents
  • Enzyme Inhibitors
  • Luminescent Proteins
  • Proteins
  • RNA, Messenger
  • X-Linked Inhibitor of Apoptosis Protein
  • Green Fluorescent Proteins
  • Methylnitrosourea