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Gene expression data from primary human hepatocytes treated with idelalisib for 24 h

ABSTRACT: Gene expression data from primary human hepatocytes treated with idelalisib for 24 h

PROVIDER: PRJNA561144 | ENA |

REPOSITORIES: ENA

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Gene expression data from primary human hepatocytes treated with idelalisib for 24 h

Project description:Idelalisib is a phosphatidylinositol 3-delta kinase inhibitor that has shown good efficacy in treating some hematologic malignancies. Rare, but potentially serious liver toxicity was associated with idelalisib use in clinical trials. The objective of this study was to evaluate the idelalisib-induced activation of stress response pathways in human hepatocytes to inform mechanisms of liver injury observed in the clinic Primary human hepatocytes from three donors were sandwich cultured and assayed for global gene expression across 5 concentrations of idelalisib after a 24 h exposure. The most significantly enriched pathway among genes upregulated in response to idelalisib was “Endoplasmic Reticulum Stress”. These data suggest that oxidative stress is a dominant mechanism contributing to liver injury associated with idelalisib.

2022-08-20 | GSE136059 | GEO

Primary Mouse Hepatocytes treated with 500μM Metformin for 24 hours

Project description:Anaylsis of gene expression in primary mouse hepatocytes treated with 500μM Metformin for 24 hours

2019-12-08 | GSE138087 | GEO

Primary Mouse Hepatocytes treated with 500μM Metformin for 24 hours

Project description:Primary Mouse Hepatocytes treated with 500μM Metformin for 24 hours

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Gene expression data from primary human hepatocytes treated with GGF2 for 6, 24, or 72 h or 24 h with a 48 h washout.

Project description:GGF2 is a recombinant human neuregulin-1β in development for chronic heart failure. Phase 1 clinical trials of GGF2 were put on hold when transient elevations in serum aminotransferases and total bilirubin were observed in 2 of 43 subjects receiving GGF2. However, aminotransferase elevations were modest and not typical of liver injury sufficient to result in elevated serum bilirubin. Several translational approaches were used to understand the liver response associated with GGF2. Gene expression profiling was performed in sandwich-cultured human hepatocytes treated with GGF2 (0-3760 pM) for up to 72 h. Prior cytochrome P450 induction studies had unexpectedly demonstrated suppression of cytochrome P450 3A4 (CYP3A4) mRNA in primary human hepatocytes exposed to GGF2 for 24 h. Although no direct cytotoxicity was observed in response to GGF2, the suppression of CYP3A4 transcript levels in primary hepatocyte cultures had a temporal profile consistent with the transient bilirubin elevations observed in vivo. While downregulation of CYP3A4 alone should not influence serum bilirubin levels, it was reasoned that concomitant alterations in the expression of other liver proteins, such as those involved in bilirubin transport, could help to explain the liver response.

2017-06-13 | GSE99926 | GEO

miR1908-5p primary hepatocytes

Project description:miR1908-5p primary hepatocytes

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Gene expression data from primary human hepatocytes treated with tolvaptan for 4, 24, or 72 h

Project description:A micropatterned coculture model (HepatoPac®) was used to explore the possibility that changes in exosome content precede overt necrosis in response to tolvaptan, a drug known to cause idiosyncratic drug-induced liver injury. Hepatocytes from 3 human donors were exposed to a range of tolvaptan concentrations bracketing plasma Cmax (0.01 - 50 µM) or DMSO control continuously for 4, 24, or 72 h. While ALT release was not significantly affected, tolvaptan exposure resulted in increased release of exosomal microRNA-122 (miR-122) into the medium. Microarray analysis was used to idenfity the activation of molecular stress response pathways most associated with increases in exosomal miR-122.

2017-06-10 | GSE99878 | GEO

Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control [RNA]

Project description:The transcriptomics changes induced in Primary Mouse Hepatocytes by Cyclosporin A after treatment for 24h and 48h The study investigated differential gene expression in Primary Mouse Hepatocytes mRNA following 24 and 48 hours of exposure to Cyclosporin A and solvent. Three biological replicates per compound/solvent. In total 24 arrays .

2014-07-24 | E-GEOD-55881 | biostudies-arrayexpress

Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control [miRNA]

Project description:The microRNA changes induced in Primary Mouse Hepatocytes of C57Bl6-mice by Cyclosporin A after treatment for 24h and 48h The study investigated differential microRNA expression in Primary Mouse Hepatocytes following 24 and 48 hours of exposure to Cyclosporin A and solvent. Three biological replicates per compound/six per solvent. In total 24 arrays .

2014-07-24 | E-GEOD-55880 | biostudies-arrayexpress

Effect of Idelalisib in follicular lymphoma monocultures and cocultured with follicular dendritic cells (FDC)

Project description:Follicular Lymphoma primary cells (FL) were treated with the PI3K delta inhibitor idelalisib (500nM, 48h) in the presence or absence of follicular dendritic cells We used microarrays to uncover the mechanisms underlying mechanism of resistance and sensitivity of FL to idelalisib

2020-09-15 | GSE130918 | GEO

Expression data from primary mouse hepatocytes treated with Diclofenac

Project description:Drug-induced liver injury (DILI) is an important clinical problem. Here we used a genomics approach to establish the critical drug-induced toxicity pathways that act in synergy with the pro-inflammatory cytokine tumor necrosis factor M-oM-^AM-! (TNFM-oM-^AM-!) to cause cell death of liver HepG2 cells. Transcriptomics of the cell injury stress response pathways initiated by two hepatoxicants, diclofenac and carbamazepine, revealed the endoplasmic reticulum (ER) stress/translational initiation signaling and Nrf2 antioxidant signaling as two major affected pathways, which was similar to that observed for the majority of ~80 DILI compounds in primary human hepatocytes. The ER stress was primarily related to PERK and ATF4 activation and subsequent expression of CHOP, which was all independent of TNFM-NM-1 signaling. Identical ATF4 dependent transcriptional programs were observed in primary human hepatocytes as well as primary precision cut human liver slices. Targeted RNA interference studies revealed that while ER stress signaling through IRE1M-NM-1 and ATF6 acted cytoprotective, activation of the ER stress protein kinase PERK and subsequent expression of CHOP was pivotal for the onset of drug/TNF-induced apoptosis. While inhibition of the Nrf2-dependent adaptive oxidative stress response enhanced the drug/TNF cytotoxicity, Nrf2 signaling did not affect CHOP expression. Both hepatotoxic drugs enhanced expression of the translational initiation factor EIF4A1, which was essential for CHOP expression and drug/TNFM-oM-^AM-!-mediated cell killing. Our data support a model in which enhanced drug-induced translation initiates PERK-mediated CHOP signaling in an EIF4A1 dependent manner, thereby sensitizing towards caspase-8-dependent TNF induced apoptosis. 4 biological replicates of Diclofenac and 6 biological replicates of vehicle. 46 hours after isolation, cells were exposed to either 300 M-BM-5M DCF or the solvent DMSO for 24 hours.

2014-01-22 | E-GEOD-54256 | biostudies-arrayexpress

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