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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE87526 | GEO | 2017/06/09

SECONDARY ACCESSION(S): PRJNA345019

REPOSITORIES: GEO

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

Project description: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).

2010-02-15 | GSE16643 | GEO

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

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

Project description:Treatment with glucocorticoids is known to cause ocular hypertension in humans which can lead to steriod-induced glaucoma We used microarrays to determine changes in gene expression in two human trabecular meshwork (TM) cell isolates (TM-4 and TM-2) from the same donor that could explain the increase in ocular hypertension.

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Comparison of Trabecular Meshwork-Derived Cells (TMDCs) with other somatic Cell Types

Project description:Microarray study comparing trabecular meshwork-derived cells (TMDCs) from the iridocorneal angle of the human eye, with other human cell types such as scleral fibroblasts, corneal fibroblasts, retinal pigmented epithelial (RPE) cells, corneal stroma, human embryonic stem cells (hESC), neural precursors differentiated from hESC, human umbilical vein endothelial (HUVEC) cells and human adipose-tissue-derived mesenchymal stromal cells (MSC) 19 samples were analysed, including 6 biological replicates of TMDC, 2 biological replicates of scleral fibroblasts, 3 biological replicates of hAd-MSC

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Comparison of Trabecular Meshwork-Derived Cells (TMDCs) with other somatic Cell Types

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

Project description:To identify genes whose expressions in primary human trabecular meshwork (TM) cell cultures are affected by the transcription factor PITX2 and to identify genes that may have roles in glaucoma. Expression profiles derived using microarrays were compared between TM control cells and cells treated with PITX2 siRNAs

2011-04-01 | GSE27275 | GEO

FOXC1 in human trabecular meshwork cells is involved in regulatory pathway that includes miR-204, MEIS2, and ITGβ1

Project description:To identify genes whose expressions in primary human trabecular meshwork (TM) cell cultures are affected by the transcription factorfoxc1 and to identify genes that may have roles in glaucoma. Expression profiles derived using microarrays were compared between TM control cells and cells treated with foxc1 siRNAs.

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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.

2024-06-30 | GSE236016 | GEO

Trabecular meshwork cell-derived exosomal microRNA expression

Project description:Trabecular meshwork cells in eyes with glaucoma aquire mesenchymal phenotypes. The types of microRNAs in exosomes may differ between static and glaucomatous status and their effects on aqueous humor regulation are still uknown. We used microarrays to identify the differential microRNA expression related to interaction between trabecular meshwork cells and Schlemm's canal endothelial cells.

2021-11-17 | GSE175464 | GEO

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