Effect of PPAR Gamma Agonist Rosiglitazone on Carotid Artery Gene Expression after Knockout of Retinol Binding Protein 7 (RBP7)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE88706 | GEO | 2017/08/22
SECONDARY ACCESSION(S): PRJNA348310
REPOSITORIES: GEO
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Project description:To better understand what genes are regulated by PPAR gamma, an experimental dataset was generated by microarray analysis, in duplicate, of pooled aortic mRNA isolated from adult male mice (C57BL/6J strain) treated for 21 days with a PPAR gamma agonist (rosiglitazone) or vehicle. Keywords: other
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Project description:Effect of PPAR Gamma Agonist Rosiglitazone on Carotid Artery Gene Expression after Knockout of Retinol Binding Protein 7 (RBP7)
| PRJNA348310 | ENA
Project description:To better understand what genes are regulated by PPAR gamma, an experimental dataset was generated by microarray analysis, in duplicate, of pooled aortic mRNA isolated from adult male mice (C57BL/6J strain) treated for 21 days with a PPAR gamma agonist (rosiglitazone) or vehicle.
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Project description:We examined the alternation of gene expression by MCC-555, rosiglitazone (RGZ) and 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2) in human colorectal adenocarcinoma HCT-116 cells. Keywords: effects of PPAR-gamma agonists
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Project description:Rosiglitazone-targeted transcriptional networks as gene expression signature of physiological and pathological mineralization – a top-down approach to identify novel targets for bone and vascular health Clinical studies have recently revealed detrimental skeletal and vascular effects of the insulin sensitizer rosiglitazone. At the cellular level, we have shown earlier that rosiglitazone accelerates osteoblast differentiation from human mesenchymal stem cells (hMSC) at the expense of increased oxidative stress and apoptosis. In calcifying human vascular cells, rosiglitazone stimulates pathological mineralization, an effect that was diminished by the antioxidant resveratrol. In order to elucidate the transcriptional networks underlying the rosiglitazone-enhanced mineralization phenotype, we performed genome-wide transcriptional profiling of osteogenic hMSCs treated with rosiglitazone for short-term periods of 1 up to 48h during the first two days of culture time, a phase that we show is sufficient to mediate the stimulatory effect of rosiglitazone on mineralization. Microarray-based mRNA expression analysis revealed 190 probes that were differently expressed in at least one condition compared to vehicle-treated control. This rosiglitazone gene signature contained confirmed primary PPAR targets and was also endogenously regulated during osteogenic differentiation from hMSCs and osteoblast-like differentiation of vascular smooth muscle cells (VSMCs) into calcifying vascular cells (CVCs). Further comparative analysis revealed rosiglitazone targets that were commonly enriched in osteoblasts and CVCs or specifically enriched in either osteoblasts or CVCs. Finally, we compared the expression patterns of CVC-specific genes with patient expression data from carotid plaque versus intact adjacent tissue, and identified five rosiglitazone targets that were differentially regulated in CVCs and carotid plaque but not osteoblasts when compared to their respective non-mineralizing counterparts. These targets, i.e PDK4, SDC4, SPRY4, TCF4, and DACT1 may specifically control extracellular matrix mineralization in vascular cells and hence provide interesting candidates for further investigations to improve vascular health.
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Project description:Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension. Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion. To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the gene expression patterns in mouse aorta in response to activation or interference with the PPAR gamma signaling pathway. Experiment Overall Design: To assess the response to PPAR gamma interference, we used adult mice containing a dominant negative form of PPAR gamma. These mice have a targeted P465L mutation, which is equivalent to the P467L mutant, described in human patients. Wild-type littermates were used as the genetic control. The PPAR gamma signaling pathway was activated by administration of rosiglitazone for either 2 or 14 days to adult mice (C57BL/6J strain) at a dose of 3 or 10 mg/kg/day via the food. Control mice were fed standard mouse chow. For the microarray hybridizations, 2-3 biological replicates from each experimental group were used. Biological replicates were RNA pooled from 8 different mouse aortas. All the microarray procedures were conducted at the University of Iowa DNA Core facility using standard Affymetrix protocols. In brief, approximately 3 ug of total RNA was used as input to a one-step amplification procedure to generate biotin-labeled RNA fragments for hybridization to the Affymetrix GeneChip Mouse Genome 430 2.0 array.
2008-06-16 | E-GEOD-8949 | biostudies-arrayexpress
Project description:Pharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in mesenteric vessels from SP467L mice and their control littermates using the Affymetrix mouse exon 1.0 ST array. We generated transgenic mice specifically targeting expression of mutant dominant negative human PPAR gamma (P467L) to vascular smooth muscle using a smooth muscle-specific promoter (smooth muscle myosin heavy chain or SMMHC). Mesenteric arteries were isolated from 3 male transgenic mice and 4 non-transgenic littermate controls. Total RNA was prepared using conventional methods and quality was assessed using the Bioanalyzer 2100 (Agilent Technologies). For the microarray hybridizations, each sample corresponded to mesenteric artery derived from one mouse. All procedures were conducted at the University of Iowa DNA Core facility using standard Affymetrix protocols. In brief, approximately 50 ng of total RNA was used as input to a two-step amplification procedure (NuGen, http://www.nugeninc.com/) to generate biotin-labeled RNA fragments for hybridization to the Affymetrix mouse exon 1.0 ST array.
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