Human naive T cells from peripheral blood were cultured in 24 wells coated with anti-CD3 and anti-CD28 antibodies in the presence or absence of retinoid acid, IL-12, and 1,25 (OH)2 vitamin D3. The T cells were FACS-sorted based on expression of CD3, integrin alpha4beta7, cutaneous lymphocyte antigen (CLA) and chemokine receptor 10. This serie includes microarray data from stimulated T cells under indicated conditions.
DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.
Specimen part
View SamplesPharmacological 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 thoracic aorta from SP467L mice and their control littermates using the Affymetrix Mouse Genome 430 2.0 array.
Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.
Specimen part
View SamplesTo examine the role of retinol binding protein 7 (RBP7) in PPAR gamma mediated regulation of target gene expression in the carotid artery, RNA-Seq was used to quantitate gene expression in carotid artery from both wild-type and RBP7 knockout mice after ligand-mediated activation of PPAR gamma with Rosiglitazone. Overall design: Carotid artery were removed from wild-type (WT) and RBP7 knockout (KO) mice and treated with either Rosliglitazone (ROSI, 10 uM) or vehicle DMSO (CONT) for 24 hrs.
Retinol-binding protein 7 is an endothelium-specific PPAR<b>γ</b> cofactor mediating an antioxidant response through adiponectin.
Sex, Specimen part, Treatment, Subject
View SamplesLigand-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 global gene expression profile in primary aortic endothelial cells in response to endothelial cell specific expression of a dominant negative isoform of PPAR gamma (V290M).
Endothelium-specific interference with peroxisome proliferator activated receptor gamma causes cerebral vascular dysfunction in response to a high-fat diet.
No sample metadata fields
View SamplesLigand-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.
Bioinformatic analysis of gene sets regulated by ligand-activated and dominant-negative peroxisome proliferator-activated receptor gamma in mouse aorta.
No sample metadata fields
View SamplesThe Ca2+/calmodulin-dependent kinase II is expressed in smooth muscle and believed to mediate intracellular calcium handling and calcium-dependent gene transcription. CaMKII is activated by Angiotensin-II.
Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.
Specimen part, Treatment
View SamplesWe analysed the capacity of THP-1 cells (differentiated to macrophagoid cells) to recognize RNA sequences via pattern recognition receptors in vitro. Gene expression was analysed by RNA-Microarray. Cytokine production was analysed by ELISA assays.
Human TLR8 senses UR/URR motifs in bacterial and mitochondrial RNA.
Cell line, Treatment
View SamplesTo examine molecular mechanisms of aortic valve stenosis in mice with hypertension and hypercholesterolemia, RNA-Seq was used during the developmental phase of stenosis to identify new gene targets. Overall design: Four groups of mice were studied: controls (CON), hypertensive (HT), hypercholesterolemic (HC), and HC/HT. Transgenic mice overexpressing human renin and human angiotensinogen served as the HT model and ApoE knockout mice served as the HC model. A sample size of N=4 was used for each of the four groups.
Fibrotic Aortic Valve Stenosis in Hypercholesterolemic/Hypertensive Mice.
No sample metadata fields
View SamplesThe brain renin-angiotensin system (RAS) stimulates resting metabolic rate in part through a mechanism involving suppression of the circulating RAS. This effect appears to be mediated through a reduction in angiotensin AT2 receptor (AT2R) signaling within inguinal fat. To examine the molecular mechanisms underlying this effect, mice with hyperactivity of the brain RAS (“sRA” mice, expressing human renin via the synapsin promoter and human angiotensinogen via its own promoter) and littermate controls were chronically infused with vehicle or the AT2R specific agonist, CGP-42112a (CGP, 90 ng/hr, 8 wk, sc). To identify altered signaling pathways, total RNA was isolated from inguinal adipose tissue and transcript abundance was quantitated by RNA-Seq. Overall design: Four groups of mice were studied: controls receiving either a saline infusion (CON) or a specific angiotensin type 2 receptor agonist (CON_CGP), transgenic mice with specific activation of the brain renin-angiotensin receiving either a saline infusion (SRA) or a specific angiotensin type 2 receptor agonist (SRA_CGP). A sample size of N=3-4 was used for each of the four groups.
Suppression of Resting Metabolism by the Angiotensin AT2 Receptor.
Sex, Specimen part, Cell line, Subject
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