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June 1997

Up-regulation of Glial Fibrillary Acidic Protein in the Retina of Primate Eyes With Experimental Glaucoma

Author Affiliations

From the Department of Ophthalmology & Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto (Drs Tanihara, Hangai, and Honda), the Department of Ophthalmology, Niigata University School of Medicine, Niigata (Drs Sawaguchi and Abe), and Santen Pharmaceutical Co Ltd (Drs Kageyama, and Shirasawa and Mr Nakazawa), Nara, Japan.

Arch Ophthalmol. 1997;115(6):752-756. doi:10.1001/archopht.1997.01100150754011

Objective:  To identify molecular mechanisms of retinal responses to intraocular pressure elevation in primate experimental glaucoma.

Methods:  An experimental glaucoma model was created by repeated laser trabeculophotocoagulation. After the preparation of complementary DNAs from extracted total RNAs in the retinas, polymerase chain reaction (PCR) experiments were performed for the following screening target genes: β-tubulin β2 and β5 and glial fibrillary acidic protein (GFAP). To investigate the amplified sequences derived from the PCR experiments, sequencing, subcloning, and Southern blot analysis of PCR products were performed. In addition, an immunohistochemical analysis was performed in an attempt to show the distribution of the target gene products in the retinas.

Results:  A series of PCR experiments suggested up-regulation of gene expression for GFAP but not for β-tu bulins. Sequencing of the PCR products and results of the Southern blot analysis showed that the amplified sequences were derived mainly from the target gene, GFAP, and that increased expression of GFAP was found despite the severity of glaucoma. Immunohistochemical studies also demonstrated increased expression of GFAP proteins in Müller cells and astrocytes in the retinas of primate eyes with experimental glaucoma.

Conclusion:  Our study showed up-regulation of GFAP at gene and protein levels, which suggests that glial components in the retina may contribute to the pathologic processes induced by elevated intraocular pressure.

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