April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Time-dependent Activation Of Autophagy In The Retinal Ischemia-reperfusion Injury
Author Affiliations & Notes
  • Matus Rehak
    Department of Ophthalmology, University of Leipzig, Leipzig, Germany
    Department of Ophthalmology, Doheny Eye Institute, University of Southern California, Los Angeles, California
  • Sindhu Saraswathy
    Department of Ophthalmology, Doheny Eye Institute, University of Southern California, Los Angeles, California
  • MinHee K. Ko
    Department of Ophthalmology, Doheny Eye Institute, University of Southern California, Los Angeles, California
  • Narsing A. Rao
    Department of Ophthalmology, Doheny Eye Institute, University of Southern California, Los Angeles, California
  • Footnotes
    Commercial Relationships  Matus Rehak, None; Sindhu Saraswathy, None; MinHee K. Ko, None; Narsing A. Rao, None
  • Footnotes
    Support  NEI EY017347 and EY 019506
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 18. doi:
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      Matus Rehak, Sindhu Saraswathy, MinHee K. Ko, Narsing A. Rao; Time-dependent Activation Of Autophagy In The Retinal Ischemia-reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2011;52(14):18.

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

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Abstract

Purpose: : Recent studies suggested that autophagy plays a role in a neural death pathway after ischemia, but the role of autophagy in retinal damage resulting from ischemia-reperfusion (IR) is not known. We investigated the time-dependent changes in the activation of autophagy in the murine model of IR.

Methods: : Unilateral retinal IR was induced in 55 adult C57BL/6 mice by cannulating the anterior chamber of the globe and transiently elevating the intraocular pressure for 60 min. Untreated eyes served as controls. After day 1, 2 and 7 of reperfusion the animals were sacrificed and the markers of autophagy as light chain 3 (LC3-I and II), beclin-1 and autophagy-related gene 5 (atg-5) were investigated using western blot techniques and immunohistochemistry. Further, the gene expression of LC3 and beclin-1 was investigated by using real-time PCR.

Results: : Retinal ischemia resulted in a rapid activation of autophagy presented by significant increase of LC3-II, beclin-1 and atg-5 detected by western blotting. The highest amount of LC3-II and atg-5 was found on day 1 after IR whereas the presence of beclin-1 protein increased continuously from day 1 to day 7 after IR. The gene expression of LC3 and beclin1 reached the highest upregulation on day 1 after IR and decreased gradually in subsequent days. But compared to untreated control eyes on day 7 there was still significant upregulation of these genes.

Conclusions: : Our study showed that the autophagy is activated after retinal ischemia-reperfusion injury. Such activation was prominent on day 1, however, there was some level of autophagic activity day 7 after retinal ischemia suggesting that autophagy could play a role in ischemic damage of the retina.

Keywords: ischemia • apoptosis/cell death • retina 
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