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Trabecular meshwork cell-derived exosomal microRNA expression

ABSTRACT: 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.

ORGANISM(S): synthetic construct Macaca mulatta

PROVIDER: GSE175464 | GEO | 2021/11/17

REPOSITORIES: GEO

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Transcription profiling of human trabecular meshwork cells after TGF-beta1 and 2 treatment

Project description:TGF-beta levels are known to increase in the aqueous humor of eye cells in patients with glaucoma. Increase TGF-beta is assumed to have a biochemical impact on the trabecular meshwork, and an increase in extracellular matrix formation, which may be responsible for decrease outflow facility of the eye. This may increase extracellular pressure, causing glaucoma. TGF-beta 1 may be the cause of abnormal accumulation of extracellular matrices in trabecular meshwork of eyes with primary open angle glaucoma. Transforming growth factor (TGF)-beta2 regulates the expression of proteoglycans in aqueous humor from human glaucomatous eyes. To identify gene expression changes as a result of TGF-beta1 and 2 treatment of human trabecular meshwork cells. We expect to see a change in expression of the proteoglycans in HTM cells as a response to TGF-beta treatment. Human Trabecular Meswork cells in the eye were bathed by aqueous humor. TM cells were removed from individuals with the following ages: 16,66,67,73, and 76. Each individual was treated with EtOH (control), TGF-beta1, or TGF-beta2. Total RNA from each individual was pooled for each chip. Technical replicates were created for each treatment type, for a total of 6 chips.

2008-06-15 | E-GEOD-7144 | biostudies-arrayexpress

TGF-beta1 and 2 treatment of human trabecular meshwork cells (Russell-3U24NS043571-01S1-2)

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Comparison of extracellular vesicle proteome between glaucoma and non-glaucoma trabecular meshwork cells

Project description:Extracellular matrix (ECM) materials accumulate in the trabecular meshwork (TM) tissue of patients with glaucoma, which is associated with a decrease in aqueous humor outflow and therefore an increase in intraocular pressure. To explore a potential mechanism for ECM regulation in the TM, we purified extracellular vesicles (EVs) from conditioned media of differentiated TM cells in culture isolated from non-glaucomatous and glaucomatous human donor eyes. EVs were purified using the double cushion ultracentrifugation gradient method. Fractions containing EV markers CD9 and TSG101 were analyzed using nanoparticle tracking analysis to determine their size and concentration. We then determined their proteomic cargo by mass spectrometry and compared protein profiles of EVs between normal and glaucomatous TM cells using PANTHER. Key protein components from EV preparations were validated with Western blotting. Results showed changes in the percentage of ECM proteins associated with EVs from glaucomatous TM cells compared to non-glaucomatous TM cells (5.7% vs 13.1% respectively). Correspondingly, we found that two ECM-related cargo proteins found across all samples, fibronection and EDIL3 were significantly less abundant in glaucomatous EVs (<0.3 fold change across all groups) compared to non-glaucomatous EVs. Overall, these data establish that ECM materials are prominent cargo in EVs from TM cells, and their binding to EVs is diminished in glaucoma

2024-01-26 | PXD044913 | Pride

Genome-wide DNA methylation in cultured human Schelmm's Canal endothelial cells and trabecular meshwork cells with or without glaucoma

Project description:Genome-wide DNA methylation profiling in cultured human Schelmm's Canal endothelial cells (SC) and trabecular meshwork (TM) cells derived from post-mortem eyes with or without glaucoma. Our study aimed to identify glaucoma-associated genes that were affected by DNA methylation.

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Autophagy the key player in trabecular meshwork death-mechanistic difference in early and advanced glaucoma

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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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2007-09-28 | E-GEOD-492 | biostudies-arrayexpress

Effects of dexamethasone for primary trabecular meshwork cell gene expression

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RNA-Seq Transcriptomic Analysis of Human Trabecular Meshwork Explants Exposed to TGF-β2: A Novel Approach Beyond Traditional Cell Culture Models

Project description:Glaucoma is a progressive optic neuropathy that can lead to irreversible blindness. Its main risk factor is elevated intraocular pressure (IOP). The trabecular meshwork (TM) acts as a filter between the anterior chamber of the eye and the aqueous humor collecting ducts, and dysfunction of this meshwork is responsible for the increased IOP in primary open-angle glaucoma (POAG). Considering that the culture conditions of human TM cells (HTMC) influence gene expression, we used human TM explants (HTMEx), which most closely mimic physiological conditions, to study the transcriptome of HTMC. The transforming growth factor-beta 2 (TGF-β2) signaling pathway has been implicated in the pathophysiology of POAG. To better characterize the role of TGF-β2 in this pathophysiology, we used bulk RNA sequencing and immunohistological analyses to establish gene signatures of TGF-β2-exposed HTMEx and correlate them with morphological alterations. We identified differentially upregulated genes primarily involved in ECM regulation, as well as profibrotic TGF-β signaling pathways, confirmed using confocal microscopy to highlight changes in trabecular architecture, TGFβ2-induced F-actin rearrangements, and extracellular matrix (ECM) deposition. Enrichment analysis also revealed modulations of gene expression related to cytoskeletal organization, as well as activation of the bone morphogenic protein (BMP) and Wnt signaling pathways in response to TGF-β2.

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Effects of dexamethasone for primary trabecular meshwork cell gene expression

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