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H. A. Quigley, Z. Yang, J. Qian, M. E. Pease, Y. Yang, D. Zack; Changes in Gene Expression in Experimental Glaucoma and Optic Nerve Transection. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3279.
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© ARVO (1962-2015); The Authors (2016-present)
We studied gene expression changes in rats after experimental intraocular pressure elevation and optic nerve transection to elucidate molecular mechanisms of retinal ganglion cell (RGC) death.
Translimbal laser photocoagulation was used to induce unilateral IOP elevation in 36 albino Wistar rats. In 36 additional animals, unilateral transection of the optic nerve was performed. Retinas were harvested 1 day, 3 days, 1 week, 2 weeks, 4 weeks, and 8 weeks after laser treatment, and total RNA was isolated with Trizol. Pooled of RNA from each time point was analyzed with Affymetrix rat genome 230 2.0 arrays. Array results were confirmed by real time PCR, and localization studies were performed using in situ hybridization and immunohistochemistry for genes of interest.
Genes that were upregulated in glaucoma, but not after transection, included Cyclin D2, Stat3, Fos, JunB, and CCAAT/enhancer binding protein. In both glaucoma and transection models, upregulation of c-Jun, Activating transcription factor 3, Heat shock protein 27, Timp1, and Annexins 1, 2, and 3 were observed. Comparisons among microarray databases were performed between our data and reports of retinal and optic nerve injury models in mice, rats, and monkeys. This analysis supports the involvement of c-Jun N-terminal kinase as a signaling molecule and the participation of tumor necrosis factor alpha in glaucoma injury.
Gene expression changes that are specific to experimental glaucoma injury were identified, including those likely to be both protective and detrimental to survival of RGC.
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