May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Overexpression of Interleukin–6 (IL–6) Through Activation of Nuclear Factor–kappa B (NF–B) in Rat Retinas Following Retinal Ischemia–Reperfusion Injury.
Author Affiliations & Notes
  • J.T. Wang
    Ophthalmology, Doheny Eye Insitute/University of Southern California, Los Angeles, CA
    Ophthalmology, The first affiliated hospital, Zhongshan University, Guangzhou, China
  • R. Sanchez
    Ophthalmology, Doheny Eye Insitute/University of Southern California, Los Angeles, CA
  • A.A. Sadun
    Ophthalmology, Doheny Eye Insitute/University of Southern California, Los Angeles, CA
  • T.T. Lam
    Ophthalmology, Doheny Eye Insitute/University of Southern California, Los Angeles, CA
  • Footnotes
    Commercial Relationships  J.T. Wang, None; R. Sanchez, None; A.A. Sadun, None; T.T. Lam, None.
  • Footnotes
    Support  NIH Core Grant EY03040 and an unrestricted grant from RPB
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3262. doi:
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      J.T. Wang, R. Sanchez, A.A. Sadun, T.T. Lam; Overexpression of Interleukin–6 (IL–6) Through Activation of Nuclear Factor–kappa B (NF–B) in Rat Retinas Following Retinal Ischemia–Reperfusion Injury. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3262.

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

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Abstract

Abstract: : Purpose: The aim of this study was to investigate the role of NF–ΚB in overexpression of IL–6, previously shown to be neuroprotective in retinal ischemia–reperfusion (I/R) injury, in rat retina after retinal I/R injury.Methods: Retinal ischemia in adult Lewis albino rats was induced by elevating the intraocular pressure to 110 mmHg for 1 hour. Animals were euthanized at 2, 4, 8, 12, 18, 24, or 48 hours after the insult. Eyes were enucleated for immunohistochemical and semiquantitative real–time RT–PCR studies of NF–ΚB, IΚB–α (endogenous inhibitor of NF–ΚB) and IL–6. Two inhibitors of NF–ΚB, helenalin and MG–132, were given to animals to examine the role of NF–ΚB activation in IL–6 production after the insult.Results: Immunoreactivity (IM) of NF–ΚB and phospho–IΚB–α (deactivated endogenous NF–ΚB inhibitor) increased in the retinal ganglion cell layer (RGCL), the inner plexiform layer (IPL) and the inner nuclear layer (INL) showing maximum expressions at 8 and 12 hours respectively after the insult. NF–ΚB and IL–6 co–localized in microglia/macrophage–like cells in the inner retina, which were also marked by ED1 antibody. Phospho–IΚB–α co–localized with ED1 in the same cells. Semiquantitative real–time RT–PCR showed elevated NF–ΚB mRNA (n=4) levels at 4 hours, coinciding with elevated IL–6 mRNA (n=4) levels at a similar time. IΚB–α mRNA (n=4) showed elevated levels at 8 hours, compared with that of normal (n=4). Helenalin and MG–132 inhibited the expression of IL–6 mRNA as measured at 4 hours after I/R injury, when IL–6 mRNA was elevated after the insult. MG–132 also inhibited NF–ΚB mRNA expression, but there was no change for NF–ΚB mRNA with helenalin.Conclusions: After retinal I/R injury, overexpression of IL–6 by microglia/macrophage–like cells is regulated by the upregulation of NF–ΚB and phosphorylation of IΚB–α.

Keywords: ischemia • neuroprotection • retina 
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