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Effects of dexamethasone for primary trabecular meshwork cell gene expression

ABSTRACT: To clarify the effects of dexamethasone treatment for primary trabecular meshwork cell gene expression, which may relates to the pathophysiology of glucocorticoid-induced glaucoma

ORGANISM(S): Homo sapiens

PROVIDER: GSE65240 | GEO | 2015/01/24

SECONDARY ACCESSION(S): PRJNA273475

REPOSITORIES: GEO

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Effects of dexamethasone for primary trabecular meshwork cell gene expression

Project description:To clarify the effects of dexamethasone treatment for primary trabecular meshwork cell gene expression, which may relates to the pathophysiology of glucocorticoid-induced glaucoma Three lots (lot #2584, 3423 and 4973) of primary culture human trabecular meshwork (TM) cells were purchased from ScienCell Research Laboratories (Carlsbad, CA). The TM cells were treated with and without 100nM dexamethasone (DEX) for 14 days. Genomewide gene expression analysis was carried out using Agilent 8X60K array.

2015-01-24 | E-GEOD-65240 | biostudies-arrayexpress

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Dexamethasone induced gene expression changes in the human trabecular meshwork

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GPR158 Activates Cellular Stress Responses in Trabecular Meshwork Cells of the Eye’s Aqueous Outflow Pathways: Implications for Ocular Hypertension

Project description:Background: the major risk factor for glaucoma is ocular hypertension, a disorder caused by reduced outflow of aqueous humor through the trabecular meshwork. In a previous pharmacogenomic screen for genes associated with ocular hypertension, we identified the novel G protein-coupled receptor, GPR158, and showed it protects against age-related ocular hypertension in mice. Here we show that the glucocorticoid, dexamethasone, increases the level of accumulated GPR158 protein in the trabecular meshwork of the human eye, ex vivo. Methods: we performed gene expression microarray profiling of TM-1 cells thar overexpress GPR158 Results: we show that the glucocorticoid, dexamethasone, increases the level of accumulated GPR158 protein in the trabecular meshwork of the human eye, ex vivo. Gene sets controlled by dexamethasone, TGFB1 and TP53 were identified, as well as genes asso-ciated with ossification. GPR158 over-expression in cells of the immortalized trabecular meshwork cell line TM-1 did not affect the fibrotic response to dexamethasone or cause ossification, and loss of GPR158 in knockout mice did not affect the development of glucocorticoid-induced ocular hypertension. However, GPR158 over-expression was cytoprotective. Discussion: Our findings suggest that GPR158 activated the cytoprotective branch of the unfolded protein response and bound the TP53-inducible protein PPP1R10, a regulatory subunit of PPI regulatory subunit of PPI. Our data support the idea that GPR158 protects the trabecular meshwork, and suggest possible mechanisms.

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