Effects of dexamethasone and KLA on HepG2 gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE278602 | GEO | 2025/04/11
REPOSITORIES: GEO
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Project description:Effects of dexamethasone and KLA on HepG2 gene expression
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Project description:Despite decades of clinical use, mechanisms of glucocorticoid resistance are poorly understood. We treated primary murine T lineage acute lymphoblastic leukemias (T-ALLs) with the glucocorticoid dexamethasone (DEX) alone and in combination with the pan-PI3 kinase inhibitor GDC-0941 and observed a robust response to DEX that was modestly enhanced by GDC-0941. Continuous in vivo treatment invariably resulted in outgrowth of drug-resistant clones, ~30% of which showed markedly reduced glucocorticoid receptor (GR) protein expression. A similar proportion of relapsed human T-ALLs also exhibited low GR protein levels. De novo or pre-existing mutations in the gene encoding GR (Nr3c1) occurred in relapsed clones derived from multiple independent parental leukemias. CRISPR/Cas9 gene editing confirmed that loss of GR expression confers DEX resistance. Exposing drug-sensitive T-ALLs to DEX in vivo altered transcript levels of multiple genes, and this response was attenuated in relapsed T-ALLs. These data implicate reduced GR protein expression as a frequent cause of glucocorticoid resistance in T-ALL.
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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.
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Project description:Analysis of dexamethasone-stimulated A549 lung adenocarcinoma epithelial cells treated with a glucocorticoid response (GR) element (GRE) specific DNA binding polyamide. Polyamide designed to target the sequence 5'-WGWWCW-3' and disrupt GR-mediated gene expression. Effects of the GR antagonist mifepristone also examined.
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Project description:The functions of human testicular peritubular cells (HTPCs), which form a small compartment located between the seminiferous epithelium and the interstitials areas of the testis, go beyond intratesticular sperm transport and include immunological roles. The expression of the glucocorticoid receptor (GR/NR3C1) by these cells indicates that they are a target of glucocorticoids (GCs), yet detailed insights into consequences of GC actions are unknown. To address this point, we studied cultured HTPCs, which serve as a window into the human testis. We used a cytokine profiler assay to screen for changes in secreted cytokines upon dexamethasone (Dex) treatment and employed qPCR and ELISA studies to verify the results. Dex, used in a therapeutic concentration, decreased proinflammatory factors, including IL6, IL8, MCP1 and CXCL1 within 24 - 48 h. An siRNA-mediated knockdown of GR reduced these actions. Exposure to Dex resulted in reduced GR levels, implying that exposure to Dex could also reduce anti-inflammatory actions of Dex. To evaluate the influence of Dex on HTPCs further, we performed a proteomic analysis of cellular components and secreted proteins. Strong responses were detectable after 24 h (31 significantly altered cellular proteins) and more pronounced ones after 72 h (30 less abundant and 42 more abundant cellular proteins). Dex also altered the composition of the secretome (33 proteins decreased, 13 increased) after 72 h. Among the regulated proteins were ECM- and basement membrane components (e.g. FBLN2, COL1A2, COL3A1), as well as PTX3 and StAR. These results reveal that Dex via GR exerts profound actions in HTPCs. If transferrable to the human testis, changes specifically in ECM and the immunological state of the testis may result in men upon treatment with Dex for medical reasons. -Secretome Data Subset-
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Project description:The functions of human testicular peritubular cells (HTPCs), which form a small compartment located between the seminiferous epithelium and the interstitials areas of the testis, go beyond intratesticular sperm transport and include immunological roles. The expression of the glucocorticoid receptor (GR/NR3C1) by these cells indicates that they are a target of glucocorticoids (GCs), yet detailed insights into consequences of GC actions are unknown. To address this point, we studied cultured HTPCs, which serve as a window into the human testis. We used a cytokine profiler assay to screen for changes in secreted cytokines upon dexamethasone (Dex) treatment and employed qPCR and ELISA studies to verify the results. Dex, used in a therapeutic concentration, decreased proinflammatory factors, including IL6, IL8, MCP1 and CXCL1 within 24 - 48 h. An siRNA-mediated knockdown of GR reduced these actions. Exposure to Dex resulted in reduced GR levels, implying that exposure to Dex could also reduce anti-inflammatory actions of Dex. To evaluate the influence of Dex on HTPCs further, we performed a proteomic analysis of cellular components and secreted proteins. Strong responses were detectable after 24 h (31 significantly altered cellular proteins) and more pronounced ones after 72 h (30 less abundant and 42 more abundant cellular proteins). Dex also altered the composition of the secretome (33 proteins decreased, 13 increased) after 72 h. Among the regulated proteins were ECM- and basement membrane components (e.g. FBLN2, COL1A2, COL3A1), as well as PTX3 and StAR. These results reveal that Dex via GR exerts profound actions in HTPCs. If transferrable to the human testis, changes specifically in ECM and the immunological state of the testis may result in men upon treatment with Dex for medical reasons. -Proteome Data Subset 24 h-
2023-03-11 | PXD033514 | Pride
Project description:The functions of human testicular peritubular cells (HTPCs), which form a small compartment located between the seminiferous epithelium and the interstitials areas of the testis, go beyond intratesticular sperm transport and include immunological roles. The expression of the glucocorticoid receptor (GR/NR3C1) by these cells indicates that they are a target of glucocorticoids (GCs), yet detailed insights into consequences of GC actions are unknown. To address this point, we studied cultured HTPCs, which serve as a window into the human testis. We used a cytokine profiler assay to screen for changes in secreted cytokines upon dexamethasone (Dex) treatment and employed qPCR and ELISA studies to verify the results. Dex, used in a therapeutic concentration, decreased proinflammatory factors, including IL6, IL8, MCP1 and CXCL1 within 24 - 48 h. An siRNA-mediated knockdown of GR reduced these actions. Exposure to Dex resulted in reduced GR levels, implying that exposure to Dex could also reduce anti-inflammatory actions of Dex. To evaluate the influence of Dex on HTPCs further, we performed a proteomic analysis of cellular components and secreted proteins. Strong responses were detectable after 24 h (31 significantly altered cellular proteins) and more pronounced ones after 72 h (30 less abundant and 42 more abundant cellular proteins). Dex also altered the composition of the secretome (33 proteins decreased, 13 increased) after 72 h. Among the regulated proteins were ECM- and basement membrane components (e.g. FBLN2, COL1A2, COL3A1), as well as PTX3 and StAR. These results reveal that Dex via GR exerts profound actions in HTPCs. If transferrable to the human testis, changes specifically in ECM and the immunological state of the testis may result in men upon treatment with Dex for medical reasons. -Proteome Data Subset 72 h-
2023-03-11 | PXD033534 | Pride
Project description:Glucocorticoid resistance (GCR), i.e. unresponsiveness to the beneficial anti-inflammatory activities of the glucocorticoid receptor (GR), poses a serious problem in the treatment of inflammatory diseases. One possible solution to try and overcome GCR, is to identify molecules that prevent or revert GCR by hyper-stimulating the biological activity of the GR. To this purpose, we screened for compounds that potentiate the dexamethasone (Dex)-induced transcriptional activity of GR. To monitor GR transcriptional activity, the screen was performed using the lung epithelial cell line A549 in which a glucocorticoid responsive element (GRE) coupled to a luciferase reporter gene construct was stably integrated. Histone deacetylase inhibitors (HDACi) such as Vorinostat and Belinostat are two broad-spectrum HDACi that strongly increased the Dex-induced luciferase expression in our screening system. In sharp contrast herewith, results from a genome-wide transcriptome analysis of Dex-induced transcripts using RNAseq, revealed that Belinostat impairs the ability of GR to transactivate target genes. The stimulatory effect of Belinostat in the luciferase screen further depends on the nature of the reporter construct. In conclusion, a profound discrepancy was observed between HDACi effects on two different synthetic promoter-luciferase reporter systems. The favorable effect of HDACi on gene expression should be evaluated with care, when considering them as potential therapeutic agents.
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