November 1998
Volume 39, Issue 12
Free
Articles  |   November 1998
Autoantibodies to small heat shock proteins in glaucoma.
Author Affiliations
  • G Tezel
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
  • G M Seigel
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
  • M B Wax
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Investigative Ophthalmology & Visual Science November 1998, Vol.39, 2277-2287. doi:
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      G Tezel, G M Seigel, M B Wax; Autoantibodies to small heat shock proteins in glaucoma.. Invest. Ophthalmol. Vis. Sci. 1998;39(12):2277-2287.

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

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Abstract

PURPOSE: To identify the low-molecular-weight retinal proteins that are the targets of serum autoantibodies in patients with glaucoma and to study the ability of these antibodies to induce retinal apoptosis. METHODS: Serum immunoreactivity against retinal proteins was examined in age-matched groups of 60 patients with normal-pressure glaucoma, 36 patients with high-pressure glaucoma, and a control group of 20 healthy subjects, by means of western blot analysis and enzyme-linked immunosorbent assay. The specificity of the immunoreactivity to small heat shock proteins, including alpha-crystallins and hsp27, was tested by immunoprecipitation of these proteins in retinal fractions. The direct effects of antibodies specific to small heat shock proteins were then studied in isolated intact human retina (ex vivo) and cultured rat retinal cells (in vitro) by immunocytochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) technique in conjunction with fluorescence microscopy and confocal imaging. RESULTS: Serum immunoreactivity against retinal proteins with low molecular weight in patients with glaucoma was to small heat shock proteins, including alpha-crystallins and hsp27. In addition, patients with normal pressure glaucoma had a higher titer of autoantibodies to small heat shock proteins than did age-matched patients with high-pressure glaucoma or control subjects. It was observed that when antibodies against small heat shock proteins were applied directly to retina tissue or cells, they could trigger cell death through an apoptotic mechanism. CONCLUSIONS: These findings suggest that increased titers of circulating antibodies against retinal small heat shock proteins may have pathogenic significance in some patients with glaucomatous optic neuropathy.

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