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K. Hori, A. Matsuda, K. Imai, K. Mori, J. Hamuro, S. Kinoshita, A. Murakami; The Roles of Plasminogen Activator Inhibitor-1 for the Pathogenesis of Atopic Cataracts. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2620.
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We previously showed an association between interferon-gamma (IFN-γ) receptor polymorphisms and occurrence of atopic cataracts (IOVS 48:583-589, 2007). A recent study showed that IFN-γsignal is essential for PAI-1 induced post-operative fibrosis in abdomen (Nat Med. 14:437-441, 2008). In this study we further tried to clarify the roles of a fibrosis related protein, Plasminogen Activatior Inhibitor-1 (PAI-1), for the pathogenesis of atopic cataracts.
Realtime-PCR analysis was carried out to compare the PAI-1 mRNA expression between the cDNA samples obtained during cataract surgery from the lens epithelium of atopic cataracts (n=10) and of senile cataracts(n=10). Cultured lens epithelial cells were stimulated by recombinant IFN-γ, and compared PAI-1 expression by real time PCR and Western blotting. Immunohistochemical analysis was carried out using the anterior capsular tissue obtained from atopic cataracts.
The relative expression of PAI-1 mRNA was significantly higher in the cDNA samples obtained from atopic cataracts compared to those from senile cataracts. Recombinant IFN-γ stimulation induced 4.6-fold higher PAI-1 mRNA expression in cultured lens epithelial cells at 24 hours after stimulation. PAI-1 positive immunostaining was observed at the subcapsular fibrosis of atopic cataracts.
Our results suggested that IFN-γ- PAI-1 signaling cascade plays some roles for the pathophysiology of atopic cataracts.
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