Autophagy induction does not protect retina against apoptosis in ischemia/reperfusion model

Adv Exp Med Biol. 2014:801:677-83. doi: 10.1007/978-1-4614-3209-8_85.

Abstract

The role played by autophagy after ischemia/reperfusion (I/R) in the retina remains unknown. Our study investigated whether ischemic injury in the retina, which causes an energy crisis, would induce autophagy. Retinal ischemia was induced by elevation of the intraocular pressure and modulation of autophagic markers was analyzed at the protein levels in an early and late phase of recovery. Following retinal ischemia an increase in LC3BII was first observed in the early phase of recovery but did not stay until the late phase of recovery. Post-ischemic induction of autophagy by intravitreal rapamycin administration did not provide protection against the lesion induced by the ischemic stress. On the contrary, an increase in the number of apoptotic cells was observed following I/R in the rapamycin treated retinas.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Autophagy / drug effects
  • Autophagy / physiology*
  • Disease Models, Animal
  • Immunosuppressive Agents / pharmacology
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / pathology*
  • Reperfusion Injury / physiopathology
  • Retina / pathology*
  • Retinal Diseases / pathology*
  • Retinal Diseases / physiopathology
  • Sirolimus / pharmacology

Substances

  • Immunosuppressive Agents
  • Sirolimus