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Effect of glucocorticoid chemical structure and receptor potency on human trabecular meshwork cells

ABSTRACT: Glucocorticoids with different chemical structures but similar glucocorticoid receptor potency regulate subsets of common and unique genes in human trabecular meshwork cells. Gene expression changes of human trabecular meshwork cells, TM 86 and TM 93, due to treatment with dexamethasone (Dex), fluocinolone acetonide (FA), and triamcinolone acetonide (TA).

ORGANISM(S): Homo sapiens

PROVIDER: GSE16643 | GEO | 2010/02/15

SECONDARY ACCESSION(S): PRJNA116225

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

Comparison of gene expression profile of human trabecular meshwork cells induced by triamcinolone with dexamethasone

Project description:PURPOSE. Triamcinolone acetonide (TA) and dexamethasone (DEX) are corticosteroids commonly used for ocular inflammation but both can cause ocular hypertension. We investigated the differential gene expression profile of human trabecular meshwork (TM) cells in response to treatment by TA compared to that by DEX. METHODS. Total RNA was extracted from cultured human TM cells treated with TA or DEX and used for microarray gene expression analysis. The microarray experiments were repeated three times. Differentially expressed genes were identified by an empirical Bayes approach and confirmed by real-time quantitative PCR. RESULTS. 0.1 mg/ml TA treatment resulted in 15 genes up-regulated and 12 genes down-regulated while 1mg/ml TA treatment resulted in 36 genes up-regulated and 21 genes down-regulated. These genes were mainly associated with acute-phase response, cell adhesion, cell cycle and growth, growth factor, ion binding, metabolism, proteolysis and transcription factor. Two genes, MYOC and GAS1, were up-regulated and 3 genes, SENP1, ZNF343 and SOX30, were down-regulated by both TA and DEX treatment. Eight differentially expressed genes were located in known primary open angle glaucoma (POAG) loci, including MYOC, SOAT1, CYP27A1, SPOCK, SEMA6A, EGR1, GAS1 and ATP10A. CONCLUSIONS. Differential gene expression profiles of human TM cells treated by TA and DEX, and a dosage effect by TA, were revealed by microarray technology. TA and DEX treatment shared several differentially expressed genes, suggesting a common mechanism to cause ocular hypertension. Some differentially expressed genes located in the known POAG loci are potential candidates for glaucoma genes. A total of 9 samples were used for this study. There were 3 biological replicates for each of 3 treatments.

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Comparison of gene expression profile of human trabecular meshwork cells induced by triamcinolone with dexamethasone

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Global expression analysis of the trabecular meshwork, cornea, sclera and trabecular meshwork-derived mesenchymal stem cells (TM-MSC)

Project description:Microarray study comparing the trabecular meshwork (TM) with TM-MSC, corneal and scleral tissues

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Changes in Gene expression mediated by Cyclic Mechanical Stress in Trabecular Meshwork Cells

Project description:Purpose: To investigate the changes in gene expression induced by cyclic mechanical stress (CMS) in trabecular meshwork (TM) cells.

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Expression Profile of Genes in Trabecular Meshwork Cells Treated with Dexamethasone

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Effect of PITX2 knockdown on transcriptome of primary human trabecular meshwork cell cultures

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