Genome-wide DNA methylation in cultured human Schelmm's Canal endothelial cells and trabecular meshwork cells with or without glaucoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE129183 | GEO | 2020/01/03
REPOSITORIES: GEO
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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
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
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
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. Keywords: dose response
2007-02-28 | GSE7144 | GEO
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
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.
2018-12-20 | GSE124114 | GEO
Project description:Dr. Panjwani's laboratory is focusing on the mechanism by which galectins-3 and 7 mediate corneal epithelial cell migration. We are currently performing studies to: (i) identify and characterize the corneal epithelial cell surface and extracellular matrix (ECM) molecules which serve as counterreceptors of galectin-3 and -7, to establish whether the lectins modulate corneal epithelial cell migration by binding to well known integrins, growth factor receptors, and/or ECM molecules and (ii) determine whether galectin-3 mediates corneal epithelial cell migration indirectly by modulating the expression of key adhesion and/or signal transduction molecules by using small interfering RNA, cDNA microarrays and glycogene arrays. It is known that a carbohydrate-binding protein, ELAM, serves as a marker for glaucoma. Other preliminary studies in my lab have shown that galectin-8 plays a role in the adhesion and spreading of trabecular meshwork cells (TM;the cells which modulate ocular pressure) and galectin-3 influences phagocytic capacity of TM cells. These studies suggest that galectins as well as ELAM and their counterreceptors may contribute to the pathogenesis of glaucoma. We have RNA preparations of five each of normal and glaucoma TM samples harvested over the last year from cadavers. We have RNA preparations of five each of normal and glaucoma TM samples harvested over the last yeat from cadavers.
2011-02-04 | E-GEOD-27057 | biostudies-arrayexpress
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
Project description:Dr. Panjwani's laboratory is focusing on the mechanism by which galectins-3 and 7 mediate corneal epithelial cell migration. We are currently performing studies to: (i) identify and characterize the corneal epithelial cell surface and extracellular matrix (ECM) molecules which serve as counterreceptors of galectin-3 and -7, to establish whether the lectins modulate corneal epithelial cell migration by binding to well known integrins, growth factor receptors, and/or ECM molecules and (ii) determine whether galectin-3 mediates corneal epithelial cell migration indirectly by modulating the expression of key adhesion and/or signal transduction molecules by using small interfering RNA, cDNA microarrays and glycogene arrays. This study seeks the role of carbohydrate-based recognition system in the pathogenesis of glaucoma. In this study, RNA preparations of four normal and five glaucoma TM samples harvested over the last year from cadavers were hybridized and analyzed using the GLYCOv2 array. We have an NIH RO3 grant award to study the role of carbohydrate-based recognition system in the pathogenesis of glaucoma. In particular, it is known that a carbohydrate-binding protein, ELAM, serves as a marker for glaucoma. Other preliminary studies in my lab have shown that galectin-8 plays a role in the adhesion and spreading of trabecular meshwork cells (TM; the cells which modulate ocular pressure) and galectin-3 influences phagocytic capacity of TM cells. These studies suggest that galectins as well as ELAM and their counterreceptors may contribute to the pathogenesis of glaucoma. We would therefore like to compare glycogene expression patterns of normal and glaucomatous TM tissue. To this end, last month we submitted RNA preparations of five each of normal and glaucoma TM tissue harvested over the last year from cadavers. The data of these samples are now being analyzed. Meanwhile, we have analyzed RNA preparations of TM cells grown in culture from five normal and six glaucoma eyes. It is our hope that data from the two projects will enable us conclusively identify glycogenes which are differentially expressed in normal and glaucoma TM cell. Overall, the goal is to shed light on the role of carbohydrate-based recognition system and the carbohydrate-binding proteins in the pathogenesis of glaucoma.
2011-02-04 | E-GEOD-27058 | biostudies-arrayexpress
Project description:Microarray study comparing the trabecular meshwork (TM) with TM-MSC, corneal and scleral tissues
2017-06-09 | GSE87526 | GEO