AngII-regulated genes sensitive to CsA in Vascular Smooth muscle cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Vanesa Esteban
PROVIDER: E-GEOD-31321 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:We have employed whole genome microarray expression profiling as a platform to identify AngII -regulated genes sensitive to CsA. VSMC were treated with AngII with or without CsA ( as an inhibitor of the CN/NFAT pathway).
2011-08-11 | GSE31321 | GEO
Project description:Compare the gene expression in intact Ubs after treated with AngII vs. Media, determine the key genes related to the ub branching gene expression change pattern. Two condition experiments, media and AngII. Biological replicate. Two for media samples, two for AngII treatment samples.
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Project description:Proteinuria is pathogenic to proximal tubular cells (PTC) and linked with progression to renal failure. Angiotensin II (AngII) is also independently involved in the pathogenesis of progressive renal injury in varied kidney disease. The effects of human serum albumin (HSA) overload, AngII and candesartan, a specific inhibitor of AngII type 1 recptor, on the changes in gene protein expression stimulated by oxidative stress in PTC were assesed using cDNA microarrays. Keywords: stress response Cells were growth arrested for 48 h in serum-free DMEM/Ham's F-12 medium with 5.5 mM glucose, 2 mM L-glutamine,100 U/ml penicillin, 100 ug/ml streptomycin, 20 mM Hepes. Media were refreshed and cells were incubated for 24h in conditioned media alone, or with media supplemented with 30mg/ml of different HSA preparations, 1 uM AngII or AngII in the presence of candesartan. After further 24 h under standard cell culture conditions (37C, 5% CO2) cells were subjected to RNA extraction.
2010-06-25 | E-GEOD-10648 | biostudies-arrayexpress
Project description:We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure. Twelve week-old C57BL6 male mice were randomly assigned to 4 groups: 1. Control, 2. L-NAME treatment, 3. AngII treatment, 4. L-NAME+AngII treatment.L-NAME (0.3 mg/ml with 1% NaCl) was administered in drinking water. AngII (0.7 mg/kg/day) was administered via subcutaneous micro-osmotic pumps. L-NAME and AngII were administered to mice for 5 weeks and 4 weeks in combination to induce HF or alone to study the effects of the individual agents.
2016-01-19 | E-GEOD-72132 | biostudies-arrayexpress
Project description:Endothelial cell and vascular smooth muscle cell were cocultured in hanging droplets to form spheroids representing an inverted vessel lumen. Control or conditioned media from an extravillous trophoblast (EVT) cell line was incubated with vascular spheroids for 24 hours. Spheroid RNA was then analyzed by Illumina Sentrix BeadChip array. Spheroids incubated with EVT conditioned medium showed significant up/downregulation of 101 genes (>1.5-fold; P<0.05), including an upregulation of C-X-C motif chemokine 10 (IP-10). C-X-C motif chemokine 10 expression was confirmed by qualitative real-time PCR and Western blot analysis of spheroids, and immunohistochemistry of first trimester decidua and ex vivo dissected nonplacental bed spiral arteries. EVT conditioned medium reduced VSMC expression of differentiation markers, and both EVT conditioned medium and C-X-C motif chemokine 10 increased motility of VSMC indicating dedifferentiation of VSMC.
2013-02-17 | E-MTAB-1462 | biostudies-arrayexpress
Project description:THP-1 cells were differentiated to macrophages with the phorbol 12-myristate 13-acetate (PMA) for a total time of 28 hours. To understand the effects of Angiotensin II (AngII) and of AngII in the presence of the thiazolidinedione pioglitazone (Pio), after 4 hours of PMA-induced differentiation of THP-1 cells (when cells became adherent), the PMA-containing medium was supplemented with AngII (1mg/ml), AngII (1 mg/ml) with Pio (1 uM), or no supplement for another 24 hours. At this time point the cells were harvested, RNA was extracted and used for a microarray-based gene profiling analysis of THP-1 cells, under the three conditions: PMA, AngII and AngII with Pio.
2014-06-01 | E-MTAB-2320 | biostudies-arrayexpress
Project description:Vascular calcification is a complex process and has been associated with aging, diabetes, chronic kidney disease (CKD). Although there have been several studies studying the role of miRNAs (miRs) in bone osteogenesis, little is known about the role of miRs in vascular calcification and their role in the pathogenesis of vascular abnormalities. Matrix vesicles (MV) are known to play an important role in initiating vascular smooth muscle cell (VSMC) calcification. In the present study, we performed miRNA microarray analysis to identify the dysregulated miRs between MV and VSMC derived from CKD rats to understand the role of post-transcriptional regulatory networks governed by these miRNAs in vascular calcification and to uncover the differential miRNA content of MV. The percentage of miRNA to total RNA was increased in MV compared to VSMC. Comparison of expression profiles of miRNA by microarray demonstrated 33 miRs to be differentially expressed with the majority (~ 57%) of them down-regulated. Target genes controlled by differentially expressed miRNAs were identified utilizing two different complementary computational approaches Miranda and Targetscan to understand the functions and pathways that may be affected due to the production of MV from calcifying VSMC thereby contributing to the regulation of genes by miRs. We found several processes including vascular smooth muscle contraction, response to hypoxia and regulation of muscle cell differentiation to be enriched. Signaling pathways identified included MAP-kinase and wnt signaling that have previously been shown to be important in vascular calcification. In conclusion, our results demonstrate that miRs are concentrated in MV from calcifying VSMC, and that important functions and pathways are affected by the miRs dysregulation between calcifying VSMC and the MV they produce. This suggests that miRs may play a very important regulatory role in vascular calcification in CKD by controlling an extensive network of post-transcriptional targets. Compare miRNA from matrix vesicles to miRNA from vascular smooth muscle cells that gave rise to the matrix vesicles from 3 sets of MV and VSMC derived from 3 normal and 3 CKD rats
2015-06-12 | E-GEOD-68913 | biostudies-arrayexpress
Project description:Angiotensin II (AngII) is a polypeptide hormone that plays a pivotal role in the regulation of blood pressure. In vascular smooth muscle cells (VSMCs), AngII signaling results in hypertrophy, proliferation, contraction, and migration, which ultimately promote atherosclerosis and hypertensive cardiovascular diseases. Recent studies have shown that fundamental biological processes such as cell proliferation and differentiation are mediated in part by the activities of long non-protein-coding RNAs (lncRNAs). In this study, we sought to identify lncRNAs that are involved in the response to AngII-signaling. Genome-wide analysis of de novo assembled transcripts from rat vascular smooth muscle cells (VSMCs) identified novel lncRNA as well as protein-coding transcripts which have not been previously annotated. The majority of the genomic loci from which these novel transcripts are transcribed are enriched for histone H3 lysine 4 trimethylation and histone H3 lysine 36 trimethylation, two chromatin modifications that are closely associated with actively transcribed regions, further supporting these as bona fide transcripts. Compared with previously annotated rat transcripts, these novel lncRNA transcripts, on average, are shorter in length and are less abundant, consistent with reports from mice and humans. Expression analyses of transcripts from control and AngII-stimulated VSMCs reveal that AngII signaling affects the abundance of both protein-coding transcripts as well as lncRNAs transcripts. Altogether, these data provide new insights into the global effects of AngII signaling and reveal potential novel therapeutic targets for treatment of AngII-associated cardiovascular diseases. RNA-sequencing of control and AngII (3hrs)-stimulated rVSMSCs. ChIP-sequencing of H3K4me3 and H3K36me3 in control and AngII (3hrs)-stimulated rVSMCs.
2013-06-30 | E-GEOD-38056 | biostudies-arrayexpress
Project description:The genetic background of mice used in this study is mainly C57BL/6J with a small contribution from 129/Sv and DBA/2J strains. Male littermates were received continuous administration of AngII for 7 days at 0.9ug/hour. On day 7 of AngII infusion, the blood pressure of infused mice was (mmHg, mean ± SD) 156 ± 1, while the control littermates remained normotensive (106 ± 9). Keywords: other
2003-10-20 | E-GEOD-606 | biostudies-arrayexpress
Project description:The calcineurin inhibitor immunosuppressant cyclosporin A (CsA) soon gained clinical application, and became a standard of care in organ transplantation, as well as an important treatment option in a variety of autoimmune diseases. The immunosuppressive effect of CsA is mainly attributed to inhibiting calcineurin phosphatase activity, consequently favouring the inactive phosphorylated form of nuclear factor of activated T cells (NFAT). Renal toxicity is a serious adverse effect of CsA, but the underlying mechanisms are insufficiently understood. CsA has also been shown to induce episodic hypoxia (Fähling et al, 2017; doi: 10.1111/apha.12811). Here, we sought to identify molecular mechanisms of CsA nephrotoxicity.
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