Overexpression of the transforming growth factor-beta-inducible gene betaig-h3 in anterior polar cataracts.

PURPOSE: In anterior polar cataracts and the fibrosis that can occur after cataract surgery, lens epithelial cells synthesize abundant extracellular matrix molecules and transdifferentiate into myofibroblast-like cells. Transforming growth factor (TGF)-beta has been implicated as a key player in these cataractous changes. The purpose of this study was to determine whether the TGF-beta-inducible gene h3 (betaig-h3) is expressed in lens epithelial cells from patients with anterior polar cataracts and to test whether betaig-h3 is induced by TGF-beta in cultured lens epithelial cells.
METHODS: Lens epithelial cells attached to the anterior capsules of human cataractous lenses and noncataractous lenses were examined for the expression of betaig-h3 mRNA and protein using reverse transcription-polymerase chain reaction and immunohistochemical analyses. The effect of TGF-beta on betaig-h3 gene expression was also tested in human lens epithelial B-3 cells using Northern and Western blot analyses.
RESULTS: betaig-h3 mRNA was not detected in lens epithelial cells from patients with clear lenses or patients with nuclear cataracts. Significant expression of mRNA for betaig-h3 was observed in lens epithelial cells from patients with anterior polar cataracts. Immunohistochemical analysis using anti-betaig-h3 antiserum indicated that betaig-h3 protein was present within the subcapsular plaques of anterior polar cataracts. Treatment of human lens epithelial B-3 cells with TGF-beta1 led to an increase in betaig-h3 mRNA and the secretion of betaig-h3 protein into the culture medium.
CONCLUSIONS: betaig-h3 may serve as a marker for anterior polar cataracts in addition to previously known proteins, fibronectin, type I collagen, and alpha-smooth muscle actin. The functions of this protein in lens pathology need to be further investigated.