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Expression of stress-response protein 60 in lens epithelial cells in atopic cataract
1Department of Ophthalmology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.
Purpose:
To clarify the pathogenesis of atopic cataract, especially to determine if there is any relationship between autoimmunity and atopic cataract.
Methods:
We investigated the lens epithelia obtained at surgery from 12 patients (12 eyes) with atopic cataract: from 8 patients (8 eyes) with nonatopic cataract (5 with senile cataract, 2 with juvenile cataract, and one with secondary cataract due to anterior uveitis); and from 4 autopsy eyes as controls.
Results:
Histopathological findings in the lens epithelial cells from atopic and nonatopic cataract patients were essentially the same: atrophy of the cells, presence of the superimposed cells, migration of cells into the lens cortex, cytoplasmic vacuolation, and loss of cells. In an immunohistochemical study, the expression of stress-response protein 60 (srp 60), srp 27, and srp 72 was examined in the lens epithelial cells. In atopic cataract specimens, 71%-87% of the lens epithelial cells were stained with the antibody against srp 60, but the cells in nonatopic cataract and control specimens were not stained.
Conclusions:
Srp 27 and srp 72 were not expressed in any observed epithelial cells. The expression of srp 60 may reflect a protective mechanism of the epithelial cells against injury triggered by immunorelated agents. These findings suggest that the pathogenesis of degeneration of the lens epithelial cells in patients with atopic cataract may be related to autoimmunity.