May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Expression of Heme Oxygenase-1 in the Human Eye
Author Affiliations & Notes
  • M.B. Mydlarski
    Ophthalmology, McGill University, Montreal, PQ, Canada
  • J. Deschenes
    Ophthalmology, McGill University, Montreal, PQ, Canada
  • H.M. Schipper
    Neurology and Neurosurgery, McGill University, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  M.B. Mydlarski, None; J. Deschenes, None; H.M. Schipper, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 649. doi:
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      M.B. Mydlarski, J. Deschenes, H.M. Schipper; Expression of Heme Oxygenase-1 in the Human Eye . Invest. Ophthalmol. Vis. Sci. 2003;44(13):649.

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

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Abstract

Abstract: : Background: Viable cells exposed to oxyradicals undergo a ubiquitous, protective "stress response" by expressing various stress proteins. Enhanced immunoreactivity for the stress protein heme oxygenase-1 (HO-1), a marker of oxidative stress, has been found in age-related neurodegenerations, as well as the RPE in neovascular ARMD. Additionally, HO-1 induction has been demonstrated in cultured corneal and lens epithelial cells exposed to oxidative stressors. Purpose: To evaluate the distribution of HO-1 expression in the human eye and to determine whether differences in ocular HO-1 immunoreactivity become apparent with age. Methods: Paraffin sections of whole human eye tissue (Quebec Eye Bank) from 6 subjects aged 16 to 72 were prepared for immunohistochemistry and incubated with the polyclonal anti-HO-1 antibody (StressGen). Adjacent sections were similarly treated with monoclonal antibodies against GFAP. Visualization of HO-1, or GFAP, immunoreactivity as a red precipitate was achieved using 3-amino-9-ethyl-carbisol as chromogen and the Vectastain ABC technique. Treated sections were counterstained with hematoxylin, mounted, examined and photographed by light microscopy. Results: HO-1 exhibits variably moderate to strong expression in corneal epithelium. Decreased HO-1 immunoreactivity in Bowman’s layer is noted in older specimens. HO-1 immunostaining is robust in lens epithelium and is enhanced in cortical lens fibers with age. In human retina, HO-1 is over-expressed in the NFL, GCL and within the inner plexiform and photoreceptor cell layers of older macula. Aged optic nerve exhibits gliosis, evidenced by increased GFAP expression, as well as intensification of HO-1 immunoreactivity in the laminar and retrolaminar regions. Conclusions: To our knowledge, this study represents the first to evaluate expression of HO-1 in human eyes in situ. HO-1 is strongly expressed in corneal and lens epithelia. These ocular tissues are chronically exposed to UV irradiation, a known oxidative stressor. HO-1-expression in lens cortex increases with age, suggesting that UV-mediated oxidative damage plays a role in cataractogenesis. Chronic exposure to oxyradicals may underlie the observed age-related increases in HO-1 expression in the NF and GC layers of the retina, and in astrocytes of the lamina cribrosa. Optic nerve gliosis is enhanced in older subjects as previously documented in other CNS tissues. Sustained exposure of retinal nerve fiber, photoreceptor cell, and glial elements to oxidative stress may contribute to the increased susceptibility of the aging eye to ARMD and glaucomatous neuropathy.

Keywords: aging • oxidation/oxidative or free radical damage • stress response 
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