Project description:As our results suggested that metformin acts to limit mitochondrial ROS and calcium-mediated activation of IL-6, we reasoned it would likely affect other processes in alveolar macrophages triggered by exposure to particulate matter (PM). Therefore, we treated mice with metformin in the drinking water for 24 hours before we instilled PM intratracheally. We then flow-sorted alveolar macrophages from whole lung homogenates 24 hours later for transcriptomic analysis (RNA-Seq).

2018-10-05 | GSE98731 | GEO

Effecst of metformin on the human gut micorbiome

Project description:To test the effects of metformin on the human gut micorbiome, we fist collected human stool samples. We processed the samples in vitro culturing under anaerobic condition for 24 hours using the rapidAIM assay and either and cultured them with metformin, or DMSO as a control. We know that metformin can alter the human gut microbiome and were interested in better analyzing which functional proceses were altered.

2021-03-16 | PXD016427 | Pride

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

Genes Expression Analysis of Cervical Cancer-derived cells Treated with Metformin

Project description:NOD-SCID mouse were treated with metformin for 11 and 24 days, the gene expression of tumors of mice treated with metformin were compared with respect to the expression of the tumors of mouse treated with vehicle (water). We evaluated the effect of Metformin (525mg/kg/day) for two times of treatment (11 days and 24 days) upon gene expression in tumors of mice treated or not with metformin. Metformin treatment decreased of tumor growth in both treatment regimens. A complete genomic analysis of transcriptomic status after treatment with metformin revealed an impact on the overall expression of transcripts.

2025-01-31 | GSE144395 | GEO

Ribosome profiling of metformin treatment in primary murine hepatocytes in WT, Raptor Ser-Ala mutant, Tsc2-null, Raptor mutant;Tsc2-null, and Ampk-null cells

Project description:Despite being the frontline therapy for Type 2 diabetes, the mechanisms of action of the biguanide drug metformin are still being discovered. In particular, the detailed molecular interplays between the AMPK and the mTORC1 pathway in the hepatic benefits of metformin are still ill-defined. Metformin-dependent activation of AMPK classically inhibits mTORC1 via TSC/RHEB. But several lines of evidence suggest additional mechanisms at play in metformin inhibition of mTORC1. Here we investigated the role of direct AMPK-mediated serine phosphorylation of RAPTOR in a new RaptorAA mouse model, in which AMPK phospho-serine sites Ser722 and Ser792 of RAPTOR were mutated to alanine. Metformin treatment of primary hepatocytes and intact murine liver requires AMPK regulation of both RAPTOR and TSC2 to fully inhibit mTORC1, and this regulation is critical for the translational response to metformin.

2023-08-10 | GSE157050 | GEO

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