May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Upregulation of Chemokine Expression in the Retinal Vasculature in Ischemia-Reperfusion Injury
Author Affiliations & Notes
  • N. Jo
    Ophthalmology, Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • G.S. Wu
    Ophthalmology, Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • N.A. Rao
    Ophthalmology, Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • Footnotes
    Commercial Relationships  N. Jo, None; G.S. Wu, None; N.A. Rao, None.
  • Footnotes
    Support  NIH Grant EY13253.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4936. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      N. Jo, G.S. Wu, N.A. Rao; Upregulation of Chemokine Expression in the Retinal Vasculature in Ischemia-Reperfusion Injury . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4936.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: To evaluate chemokine expression at various sites in the retina after ischemia reperfusion injury, using reverse transcription-polymerase chain reaction (RT-PCR) of selected tissue obtained by laser capture microdissection. Methods: Retinal ischemia was produced Lewis rats by increasing the intraocular pressure for 75 minutes. At 3, 6, 12 and 24 hours after reperfusion, we measured the levels of monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, MIP-1ß, interleukin (IL)-8 and interferon-γ-inducible protein, 10 kDa (IP-10) mRNA expression in the ganglion cell layer (GCL), inner nuclear layer (INL), outer nuclear layer (ONL) and retinal vessels, by RT-PCR after laser capture microdissection of these retinal layers. These chemokines were further localized by immunohistochemical methods using antibodies specific to MCP-1 and MIP-1α. Leukocyte infiltration into the retina was detected using immunostain for leukocyte common antigen. Results: Ischemia reperfusion induced expression of MCP-1, MIP-1α and MIP-1ß mRNA in the retinal vessels 3 hours after reperfusion. Six hours after reperfusion these chemokines and IL-8 mRNA expression were seen in the GCL and INL. Twelve hours after reperfusion IP-10 mRNA expression was seen in the GCL and INL. Immunoreactive MCP-1 and MIP-1α were detected in GCL, INL and the retinal vessels 24 hours after reperfusion. In the ONL, chemokine mRNA expression and immunoreactivity to these were not detected at various times. Leukocyte infiltration was noted at 12 hours, increasing markedly 24 hours after reperfusion. Conclusions: Ischemia reperfusion retinal injury results in generation of highly chemotactic agents, initially in the retinal vasculature, followed by their generation in the other inner retinal layers. Such differential chemokine expression may play a role in leukocyte recruitment and selective leukocyte infiltration in the inner retina, leading to retinal damage primary localized to the ganglion cells and other inner neuronal structures.

Keywords: cytokines/chemokines • ischemia • vascular cells 
×
×

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.

×