title: Differential gene expression in glaucoma.
abstract: In glaucoma, regardless of its etiology, retinal ganglion cells degenerate and eventually die. Although age and elevated intraocular pressure (IOP) are the main risk factors, there are still many mysteries in the pathogenesis of glaucoma. The advent of genome-wide microarray expression screening together with the availability of animal models of the disease has allowed analysis of differential gene expression in all parts of the eye in glaucoma. This review will outline the findings of recent genome-wide expression studies and discuss their commonalities and differences. A common finding was the differential regulation of genes involved in inflammation and immunity, including the complement system and the cytokines transforming growth factor β (TGFβ) and tumor necrosis factor α (TNFα). Other genes of interest have roles in the extracellular matrix, cell-matrix interactions and adhesion, the cell cycle, and the endothelin system.
authors.affiliation: Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114.
authors.forename: Tatjana C
authors.initials: TC
authors.lastname: Jakobs
mesh_terms: D000818:Animals; D003165:Complement System Proteins / Q000235:genetics; D004195:Disease Models, Animal; D015870:Gene Expression / Q000502:physiology*; D055106:Genome-Wide Association Study; D005901:Glaucoma / Q000235:genetics*; D006801:Humans; D051379:Mice; D009898:Optic Disk / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D003165:Complement System Proteins