Genome-wide Expression of Trabecular Meshwork in POAG
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Yutao Liu
PROVIDER: E-GEOD-27276 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:This study compared genome-wide expression profiles of individuals with and without Primary Open-Angle Glaucoma (POAG). One POAG case (case #6 with two replicates #10 and #11) carried a Q368X myocilin mutation.
2013-08-31 | GSE27276 | GEO
Project description:The goal of this study was to contrast genome-wide gene expression profiles of cultured human trabecular meshwork (HTM) cells, to that of control and primary open angle glaucoma (POAG) HTM tissues. Total RNA from cultured HTM cells and HTM tissue dissected from control and POAG anterior segments fixed in RNA later⢠was linearly amplified with the OvationTM Biotin RNA Amplification and Labeling System and individually hybridized to Affymetrix Human Genome U133 Plus 2.0 high density microarrays. Data analysis was performed using the GeneSpring Software 7.0. Selected genes showing significant differential expression were validated by Quantitative real-time PCR in nonamplified RNA. Cultured HTM cells retained the expression of some genes characteristic of the HTM tissue, including chitinase 3-like 1 and matrix Gla protein, but demonstrated downregulation of physiologically important genes such as myocilin. POAG HTM tissue showed relatively small changes compared to that of control donors. These changes included the statistically significant upregulation of several genes associated with inflammation and acute-phase response, including selectin-E (ELAM-I), as well as the downregulation of the antioxidants, paraoxonase 3 and ceruloplasmin. Downregulation in cultured HTM cells of genes potentially relevant for outflow pathway function highlights the importance of developing new conditions for the culture of TM cells capable of preserving the characteristics of TM cells in vivo. Comparative analysis between control and POAG tissues suggests that the upregulation of inflammation-associated genes might be involved in the progression of glaucoma. Experiment Overall Design: Total RNA from three cultured HTM cells and HTM tissue dissected from three pairs of control and two pairs of POAG anterior segments fixed in RNA later⢠was linearly amplified with the OvationTM Biotin RNA Amplification and Labeling System and individually hybridized to Affymetrix Human Genome U133 Plus 2.0 high density microarrays.
2008-06-13 | E-GEOD-4316 | biostudies-arrayexpress
Project description:The goal of this study was to contrast genome-wide gene expression profiles of cultured human trabecular meshwork (HTM) cells, to that of control and primary open angle glaucoma (POAG) HTM tissues. Total RNA from cultured HTM cells and HTM tissue dissected from control and POAG anterior segments fixed in RNA later™ was linearly amplified with the OvationTM Biotin RNA Amplification and Labeling System and individually hybridized to Affymetrix Human Genome U133 Plus 2.0 high density microarrays. Data analysis was performed using the GeneSpring Software 7.0. Selected genes showing significant differential expression were validated by Quantitative real-time PCR in nonamplified RNA. Cultured HTM cells retained the expression of some genes characteristic of the HTM tissue, including chitinase 3-like 1 and matrix Gla protein, but demonstrated downregulation of physiologically important genes such as myocilin. POAG HTM tissue showed relatively small changes compared to that of control donors. These changes included the statistically significant upregulation of several genes associated with inflammation and acute-phase response, including selectin-E (ELAM-I), as well as the downregulation of the antioxidants, paraoxonase 3 and ceruloplasmin. Downregulation in cultured HTM cells of genes potentially relevant for outflow pathway function highlights the importance of developing new conditions for the culture of TM cells capable of preserving the characteristics of TM cells in vivo. Comparative analysis between control and POAG tissues suggests that the upregulation of inflammation-associated genes might be involved in the progression of glaucoma. Keywords: Cell type comparison
2006-06-21 | GSE4316 | GEO
Project description:MicroRNAs were associated with the development and progression of glaucoma. Our study aims to identify the potential miRNAs and target genes in human trabecular meshwork related to primary open-angle glaucoma (POAG).
2023-05-05 | GSE231760 | GEO
Project description:Long non-coding RNAs were associated with the development and progression of glaucoma. Our study aim to identify the potential genes in human trabecular meshwork related to primary open-angle glaucoma (POAG).
2019-09-28 | GSE138125 | GEO
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.
2023-07-03 | GSE236302 | GEO
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: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.
2008-05-01 | E-GEOD-6298 | biostudies-arrayexpress
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: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. Keywords: Differential gene expression profile
2008-05-01 | GSE6298 | GEO