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By P. Gunvant

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Invest Ophthalmol Vis Sci. 42: 1803-1811. Steely HT Jr, English-Wright SL, Clark AF. (2000). The similarity of protein expression in trabecular meshwork and lamina cribrosa: implications for glaucoma. Exp Eye Res. 70: 17-30. Sternlicht MD, Werb Z. (2001). How matrix metalloproteinases regulate cell behavior. Annu Rev Cell Dev Biol. 17:463–516. Tamm ER. The trabecular meshwork outflow pathways: structural and functional aspects. Exp Eye Res. 88 :648-55. Tanaka M, Kovalenko SA, Gong JS, Borgeld HJ, et al.

Glutathione: Chemical, Biochemical and Medical Aspects, Wiley, New York, pp. 361–374. Mercurio F, Manning AM. (1999) NF-κB as a primary regulator of the stress response. 18:6163–6171. Monnink SH, van Haelst PL, van Boven AJ,et al. (2002) Endothelial dysfunction in patients with coronary artery disease: a comparison of three frequently reported tests. J Investig Med. 50: 19-24. Myung Kuk J, Tomarev S. (2010) Expression of Myocilin Mutants Sensitizes Cells to Oxidative Stress-Induced Apoptosis: Implication for Glaucoma Pathogenesis.

118: 378–384. 2 Manipulating Glia to Protect Retinal Ganglion Cells in Glaucoma Denise M. Inman, Caroline B. Lupien and Philip J. Horner University of Washington, Seattle WA United States of America 1. Introduction Increasing evidence supports both direct and indirect roles for retinal glia in the pathogenesis of glaucoma. To complicate these roles is the realization that glial activity can be both beneficial and detrimental to the survival of retinal ganglion cells (RGCs) and their axons. The contribution of glia to glaucoma pathogenesis also varies by compartment; glia in retina react differently to disease-induced stressors than glia in the optic nerve head or in the optic nerve.

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