Intact ureteric buds gene expression with AngII treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: renfang song
PROVIDER: E-GEOD-24932 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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.
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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). 4 independent VSMC cultures (4 replicates) from aortas of C57BL/6 mice were used for each condition (1uM AngII or 1uM AngII+200ng/ml CsA).
2011-08-10 | E-GEOD-31321 | 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: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: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: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 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
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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
2008-02-28 | GSE10648 | GEO
Project description:Objective - Thoracic aortic aneurysm (TAA), a degenerative disease of the aortic wall, is accompanied by changes in the structure and composition of the aortic extracellular matrix (ECM). The ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family has recently been implicated in TAA formation. This study aimed to investigate the contribution of ADAMTS-5 to TAA development. Approach and Results - A model of aortic dilatation by angiotensin II (AngII) infusion was adopted in mice lacking the catalytic domain of ADAMTS-5 (Adamts5Δcat). Adamts5Δcat mice showed an attenuated rise in blood pressure whilst displaying increased dilatation of the ascending aorta. Interestingly, a comparison of the aortic ECM from AngII-treated wildtype and Adamts5Δcat mice revealed versican as the most up-regulated ECM protein in Adamts5Δcat mice. This was accompanied by a marked reduction of ADAMTS-specific versican cleavage products (versikine) and a decrease of low-density lipoprotein-related protein 1 (LRP1). Silencing LRP1 expression in human aortic smooth muscle cells reduced the expression of ADAMTS5, attenuated the generation of versikine but increased soluble ADAMTS-1. A similar increase in ADAMTS-1 was observed in aortas of AngII-treated Adamts5Δcat mice, but was not sufficient to maintain versican processing and prevent aortic dilatation. Conclusions - Our results support the emerging role of ADAMTS proteases in TAA. ADAMTS-5 rather than ADAMTS-1 is the key protease for versican regulation in murine aortas. Further studies are needed to define the ECM substrates of the different ADAMTS proteases and their contribution to TAA formation.
2018-05-08 | PXD009410 | Pride