Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A systems biology approach to understand the pathophysiological mechanisms of cardiac pathological hypertrophy associated with rosiglitazone

ABSTRACT: Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone, whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone and yield knowledge as to the causative nature of rosiglitazone-associated cardiac hypertrophy. Total RNA obtained from mouse Apex from LDLr-/- mice treated with High Fat diet (HF) diet as control (n=6) or HF+Pio (n=5) or HF+Rosi (n=5).

ORGANISM(S): Mus musculus

SUBMITTER: Lars Verschuren

PROVIDER: E-GEOD-48977 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

A systems biology approach to understand the pathophysiological mechanisms of cardiac pathological hypertrophy associated with rosiglitazone.

Verschuren Lars L Wielinga Peter Y PY Kelder Thomas T Radonjic Marijana M Salic Kanita K Kleemann Robert R van Ommen Ben B Kooistra Teake T

BMC medical genomics 20140617

<h4>Background</h4>Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological and molecular mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone ...[more]

PMID: 24938300

Similar Datasets

Systems biology analysis unravels complementary action of combined Rosuvastatin and Ezetimibe therapy

Project description:Transcriptomics analysis to understand both efficacy and side effects of a cholesterol lowering drug combination therapy based on biological pathways and molecular processes affected by each drug alone or in combination. We have treated ApoE*3Leiden mice, a humanized atherosclerosis model with a unique human-like response to cholesterol-lowering drugs, with RSV and EZE alone and in combination. We demonstrate that processes affected by monotherapy can be retained and enhanced by combination therapy. In addition, combination therapy also affects a number of processes which are not predictable on basis of monotherapy M-bM-^@M-^S at least when analysis is performed within the borders of statistical significance. Our data however provide clues for these M-bM-^@M-^\non-predictableM-bM-^@M-^] effects. Total RNA obtained from mouse liver from mice treated with High-Cholesterol (HC) diet as control (n=8) or HC+RSV (n=8) or HC+EZE (n=8) or HC+RSV+EZE (n=8).

2013-02-27 | E-GEOD-38688 | biostudies-arrayexpress

A systems biology approach to understand the pathophysiological mechanisms of cardiac pathological hypertrophy associated with rosiglitazone

Project description:Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone, whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone and yield knowledge as to the causative nature of rosiglitazone-associated cardiac hypertrophy.

2014-06-30 | GSE48977 | GEO

Gene expression in mouse hematopoietic stem and multi-potent progenitor cells with temporally defined divisional histories

Project description:Homeostatic hematopoietice stem cells (HSCs) with greater divisional history lose repopulating potential after very few cell divisions. Divisional history overrides both phenotype and immediate quiescence in determining functional activity. In GFP label retaining system GFP is progressively diluted when cells proceed through a cascade of divisions. We used a GFP label retaining system and performed microarray expression analyses to track the changes in the gene expression profile of bone marrow (BM) LSK cells that relates to divisional history during homeostasis. Chromatins are dynamically labeled in a double transgenic mouse (huCD34-tTA X Tet-O-H2B-GFP) by the expression of GFP tagged Histone2B. The expression is driven by a human CD34 promoter active specifically in all bone marrow (BM) hematopoietic stem and multi-potent progenitor cells. This is a pulse/chase Tet-off system where cells constantly label with GFP. Upon administration of Doxycyclin (Dox) to GFP labeled animals, further labeling is stopped during the chase period. With each round of cell division, the newly synthesized endogenous H2B will dilute H2B-GFP by one-half, whereas cells that don’t divide will retain GFP labeling. Therefore, the level of GFP reflects how many times cells have divided over the period of Dox treatment (chase). Animals were treated with Dox for 12 weeks starting at the age of 6-8 weeks. After chase, BM Lineage negative, Sca1+, Kit+ (LSK) cells with varying GFP levels were sorted for mRNA extraction. GFP levels were ranked from 0 to 4 based on the kinetic analysis of GFP fully labeled LSK cells and obvious peaks in the GFP histogram of LSK cells after Dox treatment. There is approximately 1-2 cell divisions between each level of GFP.

2014-03-20 | E-GEOD-48261 | biostudies-arrayexpress

Transcription profiling of hy5 single mutant, hyh single mutant, hy5 hyh double mutant and wild type Arabidopsis seedlings of two different ecotypes and with or without auxin treatment

Project description:Arabidopsis thaliana seedlings comprising hy5 single mutant , hyh single mutant, hy5 hyh double mutant and wild-type plants were germinated in the dark on agar medium on usual Murashig and Skoog medium (pH 5.8) without sucrose. After 3 days of germination, etiolated seedlings were transfered to light conditions in liquid media similar to previous one but without agar . After 5 hours, auxin (10 micromolar IAA) was added to all treated samples except to controls (Mock treatment). all samples were harvested after one-hour treatment and frozen for further RNA extraction. Aim of the project was to detect impact of exogenous auxin treatment on each genotype

2006-11-08 | E-MEXP-715 | biostudies-arrayexpress

RNAi profiling of Arabidopsis Col-0 plants (air control), 8 week old Col-0 plants treated for 24 hours with ethylene gas (10 ppm), and artificial microRNA knockdown mutants, amiR-ETP1/2 - interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 triggers ethylene responses in Arabidopsis

Project description:A complex interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 is essential for triggering ethylene responses in plants. The gaseous plant hormone ethylene can trigger myriad physiological and morphological responses in plants. While many ethylene signaling pathway components have been identified and characterized, little is known about the function of the integral membrane protein EIN2, a central regulator of all ethylene responses. Here, we demonstrate that Arabidopsis thaliana EIN2 is a protein with a short half-life that undergoes rapid proteasome-mediated protein turnover. Moreover, EIN2 protein accumulation is positively regulated by ethylene. We identified two F-box proteins, EIN2 TARGETING PROTEIN and 2 (ETP1 and ETP2), that interact with the EIN2 carboxyl-terminal domain (CEND), which is highly conserved and sufficient to activate most ethylene responses. Overexpression of ETP1 or ETP2 disrupts EIN2 protein accumulation, and these plants manifest a strong ethylene insensitive phenotype. Furthermore, knocking down the levels of both ETP1 and ETP2 mRNAs using an artificial microRNA (amiRNA) leads to accumulation of EIN2 protein, resulting in plants that display constitutive ethylene response phenotypes. Finally, ethylene down-regulates ETP1 and ETP2 proteins, impairing their ability to interact with EIN2. Thus, these studies reveal that a complex interplay between ethylene, the regulation of ETP1/ETP2 F-box proteins, and subsequent targeting and degradation of EIN2 is essential for triggering ethylene responses in plants. Experiment Overall Design: Six samples were analyzed. There were three treatments with two biological replicates each. The treatments are as follows: 8 week old Col-0 plants (air control), 8 week old Col-0 plants treated for 24 hours with ethylene gas (10 ppm), and artificial microRNA knockdown mutants, amiR-ETP1/2.

2009-12-05 | E-GEOD-14247 | biostudies-arrayexpress

Mus musculus

Project description:Pioglitazone, rosiglitazone and troglitazone treatment

| PRJNA90011 | ENA

Pioglitazone, rosiglitazone and troglitazone treatment

Project description:3T3-L1 cells treated 24 hours with either 0.1% DMSO, 20uM pioglitazone, 1uM rosiglitazone or 20uM troglitazone Keywords: other

2004-08-01 | GSE1458 | GEO

Transcription profiling of mouse 3T3-L1 cells treated 24 hours with either 0.1% DMSO, 20uM pioglitazone, 1uM rosiglitazone or 20uM troglitazone

Project description:3T3-L1 cells treated 24 hours with either 0.1% DMSO, 20uM pioglitazone, 1uM rosiglitazone or 20uM troglitazone

2007-10-09 | E-GEOD-1458 | biostudies-arrayexpress

Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (mRNA)

Project description:The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.

2018-05-05 | GSE68592 | GEO

Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (miRNA)

2018-05-05 | GSE68604 | GEO