Similar Datasets
Project description:Metformin on human macrophages
| PRJNA642127 | ENA
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
Project description:This experiment includes treatment of human pulmonary fibroblasts obtained from IPF patients with metformin. Since, we would like to investigate the transcriptome profile of these samples following metformin treatment. There will be two groups consist of four samples each. First group treated with metformin for 72 hours, while the second group treated with vehicle.
2019-05-14 | GSE131133 | GEO
Project description:Metformin is a front-line drug in the treatment of type-2 diabetes mellitus (T2DM). In addition to its antigluconeogenic and insulin-sensitizing properties, it has emerged as a potent inhibitor of the inflammatory response of macrophages. Specifically, metformin has been shown to reduce transcript levels of Il1b, the gene encoding the pro-inflammatory cytokine interleukin (IL)-1b, during long-term exposure of macrophages to the bacterial cell-wall component lipopolysaccharide (LPS). However, the extent to which metformin affects the early transcriptional response to LPS has never been investigated. Here, we show that metformin affects transcript levels of a large yet selective subset of LPS-responsive genes after only two hours of LPS exposure, mostly counteracting the effect of LPS rather than enhancing it. The affected genes are implicated in a variety of biological functions, in particular cellular movement and trafficking. Intriguingly, metformin affects transcript levels of Il1b at this early time point as well, but through a molecular mechanism fundamentally different from the regulation observed after longer exposure. While down-regulation of Il1b by metformin during the late stages of the LPS response has been shown to rely on stabilization of hypoxia-inducible factor (HIF)-1α and production of IL-10, Il1b inhibition at the early stage requires AMP-activated protein kinase (AMPK) activation but is independent of HIF-1α and IL-10. These results reveal an unexpected complexity in the anti-inflammatory properties of metformin and demonstrate that Il1b is down-regulated by distinct mechanisms in the early and late stages of the LPS response.
2021-08-30 | GSE131348 | GEO
Project description:The transcriptomic changes induced in the human liver cell line HepG2 by Azathriopine (250µM, Sigma-Aldrich), Furan (2mM, Sigma-Aldrich), Tetradecanoyl phorbol acetate (500nM, Sigma-Aldrich), Tetrachloroethylene (2mM, Sigma-Aldrich), Diazinon (250µM, Sigma-Aldrich) and Dmannitol (250µM, Sigma-Aldrich) during 4, 8, 24, 48 and 72hrs As a solvent control for Azathriopine, Furan, Diazinon and Tetradecanoyl phorbol acetate, DMSO was used (0.5%); As a solvent control for tetrachloroethylene, ethanol was used (0.5%); As a solvent control for D-mannitol, HBSS was used (0.5%)
2015-01-13 | GSE58235 | GEO
Project description:Bone marrow-derived macrophages, Unstimulated DMSO Bone marrow-derived macrophages, Unstimulated + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 1h DMSO Bone marrow-derived macrophages, LPS 1h + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 2h DMSO Bone marrow-derived macrophages, LPS 2h + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 4h DMSO Bone marrow-derived macrophages, LPS 4h + I-BET (GSK525762A) LPS (100 ng/mL) was purchased from Sigma. Bone Marrow-derived macrophages (BMDMs) were differentiated from C57BL/6 bone marrow using 5 ng/mL each of recombinant M-CSF and IL-3 (Peprotech) for 7 days as described (Jeffrey et al, Nature Immunology, 2006). 2 x10^6 BMDMs were treated with DMSO or 1 μM of I-BET for 30 minutes before the addition of LPS (100 ng/mL) for 1, 2 or 4h. Unstimulated control samples were incubated with I-BET only for 1 hour. 500 ng of total RNA from 3 independent samples per group was used to prepare biotin-labeled RNA using Ambion Illumina TotalPrep RNA Amplification Kit (Applied Biosystems) and hybridized to Illumina MouseRef-8 v2.0 expression BeadChip kits. The chips were scanned using Illumina BeadArray Reader.
2010-11-10 | GSE21764 | GEO
Project description:Metformin is effective for prevention or treatment of various tumors. There are a lot of studies on the underlying mechanisms of metformin as respect to its anti-tumor action. We used microarrays to detail the global programme of gene expression underlying the anti-tumor effects of metformin on LoVo cells. Human derived LoVo cells were treated with metformin (10mM) for 8 and 24h, and the control and treated cells were harvested for RNA extraction and hybridization on Affymetrix microarrays.The samples were grouped as Met8h, Met24h, Con8h, and Con24h, respectively.
2015-03-31 | E-GEOD-67342 | biostudies-arrayexpress
Project description:Fetal sheep hepatocytes were treated for 24h with metformin
2023-02-07 | GSE224387 | GEO
Project description:C57BL/6J male mice were treated with or without metformin
2022-04-20 | GSE201039 | GEO
Project description:Metformin rejuvenates adult rat oligodendrocyte progenitor cells (OPCs) allowing more efficient differentiation into oligodendrocytes and improved remyelination of CNS axons and therefore is of interest as a possible therapeutic in demyelinating diseases such as multiple sclerosis (MS). We set out to test whether metformin had a similar effect in human stem cell derived-OPCs. We assessed the suitability of human monoculture, organoid and transplantation into immunodeficient mice (chimera model) culture systems in simulating in vivo adult human oligodendrocytes, finding most close resemblance in the chimera model. Metformin increased myelin proteins and/or sheaths in all models even when human cells had fetal signatures. In the chimera model, metformin led to a marked increase in mitochondrial area both in the human transplanted cells and in the mouse axons with associated increase in transcripts related to mitochondrial function and metabolism. Human oligodendrocytes from MS brain donors treated pre-mortem with metformin also expressed similar transcripts suggesting that metformin’s brain effect is not cell-specific, altering metabolism in both oligodendrocytes and axons leading to more myelin production, in part through mitochondrial changes. This bodes well for ongoing clinical trials testing metformin for neuroprotection.
2024-12-10 | GSE282369 | GEO