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Links from GEO DataSets

Items: 6

1.

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

(Submitter supplied) 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:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
23 Samples
Download data: TXT
Series
Accession:
GSE16643
ID:
200016643
2.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4564
9 Samples
Download data
Series
Accession:
GSE6298
ID:
200006298
3.

Expression Profile of Genes in Trabecular Meshwork Cells Treated with Dexamethasone

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
18 Samples
Download data: CEL
Series
Accession:
GSE124114
ID:
200124114
4.

Transcriptional effects of glucocorticoid receptor alpha and beta signaling in zebrafish

(Submitter supplied) The glucocorticoid receptor (GR) regulates gene expression upon activation by glucocorticoid (GC) hormones. In zebrafish, two GR splice variants exist: the canonical GR α-isoform (GRα), and the GR β-isoform (GRβ). The exact function of GRb remains elusive. We have investigated the transcriptional role of GRa and GRb in the zebrafish embryo model by injecting mebryos with two splice-blocking morpholinos (one leading to knockdown of both GR α- and β-isoforms, and another targeting the alternative splicing of the GR pre-mRNA in favor of the GR β-isoform) and with GRβ mRNA (resulting in specific GRβ overexpression). more...
Organism:
Danio rerio
Type:
Expression profiling by array
Platform:
GPL15180
24 Samples
Download data: TXT
Series
Accession:
GSE63360
ID:
200063360
5.

Effects of dexamethasone for primary trabecular meshwork cell gene expression

(Submitter supplied) To clarify the effects of dexamethasone treatment for primary trabecular meshwork cell gene expression, which may relates to the pathophysiology of glucocorticoid-induced glaucoma
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL14550 GPL17077
6 Samples
Download data: TXT
Series
Accession:
GSE65240
ID:
200065240
6.

Individual-specific functional epigenomics reveals genetic determinants of adverse metabolic effects of glucocorticoids

(Submitter supplied) Glucocorticoids (GCs) are widely used as anti-inflammatory drugs, but their long-term use has severe metabolic side effects. Here, by treating multiple patient-derived adipose stem cell-derived adipocytes and iPSC-derived hepatocytes with the potent GC dexamethasone (Dex), we uncovered cell type-specific and individual-specific GC-dependent transcriptomes and glucocorticoid receptor (GR) cistromes. Patient-specific GR binding could be traced to single nucleotide polymorphisms (SNPs) that altered the binding motifs of GR or its cooperating factors. We also discovered another set of genetic variants that modulated Dex response through affecting chromatin accessibility or chromatin architecture. Several SNPs that altered Dex-regulated GR binding and gene expression controlled Dex-driven metabolic perturbations and, remarkably, predicted metabolic side-effects of GC-treated patients. These data validate a patient stem cell-based experimental framework to discover genetic variants that impact GR function and individual responses to GC drugs, with implications for developing personalized therapies.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
177 Samples
Download data: BIGWIG, HIC, TXT
Series
Accession:
GSE163061
ID:
200163061
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