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Studies on progenitor endothelial cells; exploring mechanisms for improvement of cardiovascular diseases

ABSTRACT: Transcriptomic analysis of primary CD34+ cells. CD34+ cell were induced in vitro with hypoxia (3 hours), high glucose and high glucose plus hypoxia. Subsequently, the effect of metformin (anti-diabetic drug) on all conditions was studied to take advantage of transcriptomics to prospectively explore the mechanism of this drug to reduce the risk of cardiovascular diseases in type II diabetic patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46262 | GEO | 2016/02/24

SECONDARY ACCESSION(S): PRJNA198490

REPOSITORIES: GEO

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Studies on progenitor endothelial cells; exploring mechanisms for improvement of cardiovascular diseases

Project description:Transcriptomic analysis of primary CD34+ cells. CD34+ cell were induced in vitro with hypoxia (3 hours), high glucose and high glucose plus hypoxia. Subsequently, the effect of metformin (anti-diabetic drug) on all conditions was studied to take advantage of transcriptomics to prospectively explore the mechanism of this drug to reduce the risk of cardiovascular diseases in type II diabetic patients. Total RNA isolated from 20 samples; 10 different conditions each has 2 repeats; labeled, and hybridized to Affymetrix Human Gene 1.0 ST Array.

2016-02-24 | E-GEOD-46262 | biostudies-arrayexpress

Studies on mature endothelial cells; exploring mechanisms for improvement of cardiovascular diseases

Project description:Transcriptomic analysis of primary human umbilical vein endothelial cells (HUVEC). HUVEC were treated in vitro with CoCl2 to induce hypoxia, high glucose and high glucose plus hypoxia in different intervals (1, 3, 12 hours). Subsequently, the effect of metformin (anti-diabetic drug) on all conditions was studied to take advantage of transcriptomics to prospectively explore the mechanism of this drug to reduce the risk of cardiovascular diseases in type II diabetic patients.

2014-12-03 | GSE46263 | GEO

Transcription profiling of mouse finally differentiated 3T3-L1 adipocytes treated with insulin (0 or 100nM)or metformin (0 or 2mM)for 2 and 12 hours

Project description:Finally differentiated 3T3-L1 adipocytes are treated with insulin (0 or 100nM)or metformin (0 or 2mM)for 2 and 12 hours to understand insulin and metformin(an anti-diabetic drug commonly applied for Non-Insulin Dependent Diabetes Mellitus)action in adipose tissues.

2013-01-30 | E-BAIR-8 | biostudies-arrayexpress

Metformin targets mitochondrial complex I to lower blood glucose levels

Project description:Metformin is among the most prescribed anti-diabetic drugs, but the primary molecular mechanism by which metformin lowers blood glucose levels is unknown. Previous studies have proposed numerous mechanisms by which acute metformin lowers blood glucose, including the inhibition of mitochondrial complex I of the electron transport chain (ETC). Here, we used transgenic mice that globally express the Saccharomyces cerevisiae protein NDI1 to determine whether the glucose lowering effect of acute oral administration of metformin requires inhibition of mitochondrial complex I of the ETC in vivo. NDI1 is a yeast NADH dehydrogenase enzyme that complements the loss of mammalian mitochondrial complex I electron transport function and is insensitive to pharmacologic mitochondrial complex I inhibitors including metformin. We demonstrate that NDI1 expression attenuates metformin’s ability to lower blood glucose levels under standard chow and high-fat diet conditions. Our results indicate that acute oral administration of metformin targets mitochondrial complex I to lower blood glucose.

2024-10-12 | GSE278099 | GEO

Importance of AMPK in metformin suppression of liver glucose production

Project description:Metformin is now the most widely prescribed oral anti-diabetic agent worldwide, taken by over 150 million people annually. Although metformin has been used clinically to treat type 2 diabetes for over 60 years. Its mechanism of action remains only partially understood and controversial. In particular, this includes whether AMPK plays a role in metformin suppression of liver glucose production. To address this issue, we knocked out the AMPK catalytic alpha1 and alpha 2 subunits in the liver of HFD-fed adult homozygous mice. These mice were treated with a physiological relevent metformin dose (50 mg/kg/day) for 3 weeks. Liver samples were collected.

2019-11-13 | GSE114234 | GEO

Deep sequencing analysis of miRNAs and isomiRs modulated by long-term exposure of human endothelial cells to metformin

Project description:Increasing evidence suggest anti-senescence and geroprotective roles for the glucose-lowering drug metformin. In this framework, the ability of metformin to affect the biogenesis of selected microRNAs (miRNAs) was recently suggested. IsomiRs are distinct variations of miRNA sequences, such as addition or deletion of one or more nucleotides at the 5’ and/or 3’ ends of the canonical miRNA sequence. Since no study has comprehensively assessed the miRNA signatures, including isomiR variants, affected by metformin treatment during cellular senescence, we analysed miRNA and isomiR expression in human umbilical vein endothelial cells (HUVECs) undergoing replicative senescence in presence of metformin.

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Impact of Pretreatment With Metformin on Colorectal Cancer Stem Cells (CCSC) and Related Pharmacodynamic Markers

Project description:Metformin is drug that is normally used to treat people with diabetes. New research has discovered that metformin may also kill cancer stem cells. These cancer stem cells make up only a small portion of a cancer, but may be responsible for resistance to chemotherapy or for causing recurrence of the cancer. The purpose of this study is to determine the effect of metformin on colorectal cancer tumors. The study is designed to develop the methods to test tumors for cancer stem cells and then to determine the difference between treating with metformin and not treating with metformin with regard to the cancer stem cells. This research is investigational because the effect of metformin on cancer stem cells is not known in humans. Also, in patients who are not diabetic, metformin would normally not be given prior to surgery.

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Metformin Impairs Intestinal Fructose Metabolism

Project description:Objective: To investigate the effects of metformin on intestinal carbohydrate metabolism in vivo. Method: Male mice preconditioned with a high-fat, high-sucrose diet were treated orally with metformin or a control solution for two weeks. Fructose metabolism, glucose production from fructose, and production of other fructose-derived metabolites were assessed using stably labeled fructose as a tracer. Results: Metformin treatment decreased intestinal glucose levels and reduced incorporation of fructose-derived metabolites into glucose. This was associated with decreased intestinal fructose metabolism as indicated by decreased enterocyte F1P levels and diminished labeling of fructose-derived metabolites. Metformin also reduced fructose delivery to the liver. Proteomic analysis revealed that metformin coordinately down-regulated proteins involved carbohydrate metabolism including those involved in fructolysis and glucose production within intestinal tissue. Conclusion: Metformin reduces intestinal fructose metabolism, and this is associated with broad-based changes in intestinal enzyme and protein levels involved in sugar metabolism indicating that metformin's effects on sugar metabolism are pleiotropic.

2024-04-27 | PXD041833 | JPOST Repository

Systematic investigation of dose-dependent protein thermal stability changes to uncover the mechanisms of the pleiotropic effects of metformin

Project description:Metformin is the most popular drug to treat type II diabetes. Besides lowering blood sugar, it is proven to have more beneficial effects, including extending life expectancy. However, the underlying mechanisms remain largely elusive. Here, we systematically studied the proteome thermal stability changes induced by a wide dosage range of metformin in a liver cancer cell line using the proteome integral solubility alteration (PISA) assay. This work provides valuable and unique information about the interactions between proteins and this drug, which is not able to obtain using commonly used abundance-based proteomics. The current results demonstrated that the most acceptable target of metformin responsible for lowering blood glucose levels, complex I, was stabilized only under the high-concentration metformin treatment. Intriguingly, the complex IV subunits were significantly stabilized by low concentrations of (such as 0.2 μM) metformin, indicating that the complex IV may play an important role in the sugar-lowering effect. Moreover, low-dose metformin significantly altered ribosome and histone protein stabilities, correlated with the inhibitive effect of cell proliferation by metformin. We further found that low-concentration metformin impacted mitochondrial cargo transport and vesicle transport, while high-concentration metformin affected cell redox responses and cell membrane protein sorting. Systematic investigation of metformin-induced proteome thermal stability changes provides intriguing insights into the molecular mechanisms of lowering blood sugar and the pleiotropic effects of metformin.

2024-01-11 | PXD039382 | Pride

ena-DATASET-DUNDEE-05-08-2016-18:52:13:500-38 - samples

Project description:Variation in the Glucose Transporter gene SLC2A2 is associated with glycaemic response to metformin

| EGAD00001002277 | EGA