RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE189003 | GEO | 2022/04/08
REPOSITORIES: GEO
Similar Datasets
Project description:RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension
| PRJNA781123 | ENA
Project description:Transcriptional profiling of suprarenal aorta from ApoE-/- mice (12-14 weeks old, C57BL/6J background) treated by subcutaneous pump with angiotensin II or saline for 7d, 14d and 28d. Includes Ang II-treated samples at 7d found to have dissected aneurysms. Goal was to examine gene expression in developing AAA in this model over time. Experiment Overall Design: Two condition experiment, one suprarenal aorta per array. Saline vs. angiotensin II at 3 time points, with inclusion of 3 Ang II-treated dissected. Total 35 arrays: 6 saline 7d, 6 saline 14d, 5 saline 28d, 4 Ang II 7d, 5 Ang II 14d, 6 Ang II 28d, 3 Ang II-dissected 7d.
2009-10-09 | E-GEOD-17901 | biostudies-arrayexpress
Project description:Transcriptional profiling of suprarenal aorta from ApoE-/- mice (12-14 weeks old, C57BL/6J background) treated by subcutaneous pump with angiotensin II or saline for 7d, 14d and 28d. Includes Ang II-treated samples at 7d found to have dissected aneurysms. Goal was to examine gene expression in developing AAA in this model over time.
2009-10-01 | GSE17901 | GEO
Project description:BACKGROUND: Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters. METHODS AND RESULTS: In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell. CONCLUSIONS: Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated.<br><br>Note that files GSM6179.txt and GSM6182.txt as imported from GEO are identical.
2007-12-13 | E-GEOD-420 | biostudies-arrayexpress
Project description:BACKGROUND: Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters. METHODS AND RESULTS: In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell. CONCLUSIONS: Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated. Keywords: other
2003-08-28 | GSE420 | GEO
Project description:Angiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the gene expression in this process is unclear. We used Rat Affymetrix gene array to profile Ang II-regulated gene in RVSMC and evaluated their role in VSMC dysfunction. Examined 4 samples of Rat VSMC in triplicate. Control (without Ang II treatment) and 3 samples treated with Ang II for 6h, 12h, and 24h. Compared the changes in gene expression in Ang II treated samples relative to control samples.
2012-03-23 | E-GEOD-35627 | biostudies-arrayexpress
Project description:The goals of this study is to compare the differently expressed genes in abdominal aorta tissues of Control and Ang II with or without neferine treatment. The Ang II (n=12) were randomly divided into 2 groups: Ang II , and Ang II + neferine (1 mg/kg/day) groups (n=6 for each group). Control groups (n=5) were set as control. Mouse in Control and Ang II groups were intragastrically with double distilled water (dd H2O); while mice in Ang II + neferine (1 mg/kg/day) group were intragastrically with 1 mg/kg/day of neferine for 6 weeks. Then the abdominal aorta tissues were used to identify differentially expressed genes among different groups.
2023-04-15 | GSE229199 | GEO
Project description:Angiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the role of microRNAs (miRNAs) in this process is unclear. We used small RNA deep sequencing to profile Ang II-regulated miRNAs in rat VSMC and evaluated their role in VSMC dysfunction. Sequencing results revealed several Ang II-responsive miRNAs and bioinformatics analysis showed that their predicted targets can modulate biological processes relevant to cardiovascular diseases. Examined 4 samples of Rat VSMC. Control (without Ang II treatment) and 3 samples treated with Ang II for 1h, 3h, and 24h. Compared the changes in gene expression in Ang II treated samples relative to control samples.
2012-03-23 | E-GEOD-35664 | biostudies-arrayexpress
Project description:Angiotensin II (Ang II) mediated signaling plays a key role in the development of hypertension associated target organ damages. However, the gene expression changes regulated by Ang II in the early stage of acute cerebral, cardiac, renal, vascular injury remain unclear. we investigated Ang II–mediated gene expression alteration associated with the development of early cerebral, cardiac, renal, vascular injury by microarray assay in a mouse model.
2014-07-16 | GSE59437 | GEO
Project description:Gliomas are aggressive primary brain tumors, presenting surgery limitations due to their highly infiltrative potential. The expression of Angiotensin II (Ang II) receptors in human astrocytomas was previously associated with a poor prognosis. Accordingly, this study was undertaken to reveal the molecular mechanisms underlying Ang II actions in gliomas through the transcriptomic analysis of glioma cells exposed to Ang II. C6 glioma cells were treated with Ang II and specific antagonists of AT1 and AT2. Total RNA was isolated at three and six hours intervals and submitted to oligonucleotide microarray protocol. The differentially expressed genes were obtained by paired t-tests with p<0.05 and interpreted using Venn diagrams, functional enrichment and protein interaction network analyses. Validation of microarray results was carried out through qPCR experiments of selected genes. We found a high number of significant genes with low fold changes in gene expression at the time intervals studied. These genes were regulated in a time dependent-manner, with most gene expression changes being exclusive to one of the time intervals evaluated. Our results indicated that blocking AT1 or AT2 changed the expression of genes involved in regulation of transcription, cell cycle, cell proliferation, differentiation, apoptosis, cell adhesion, cell migration, regulation of actin cytoskeleton, protein transport and protein ubiquitination. Additionally, the signaling pathways over-represented by the significant genes were ErbB, mTOR, MAPK, neurotrophin, insulin and Wnt. Finally, interactome analyses revealed hub genes associated with cell proliferation, survival, migration, transport, structural support, neurotrophin pathway, MAPK signaling and Wnt signaling. Taken together, our findings implicate Ang II-transcriptional regulation in glioma progression by means of the modulation of genes participating in protumoral functions. This transcriptome pattern is observed upon Ang II activation of either AT1 or AT2 receptors, thereby highlighting the relevance of both receptor subtypes in glioma progression. Interactome analyses disclosed hub genes regulated by Ang II which may present higher control over their networks. These genes participate in biological functions that could enhance the degree of malignancy in gliomas and thus should be further explored. C6 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum, 100 Units/ml penicillin and 100 M-BM-5g/ml streptomycin. Cells were seeded in cell culture dishes and incubated at 37M-BM-0C/ 5% CO2 until becoming confluent. Then, these cells were pre-treated (30 minutes) with either AT1 receptor antagonist (Losartan: 10-5M) or AT2 receptor antagonist (PD123319: 10-5M) followed by Ang II treatment (10-7 M) according to the treatment scheme: Group 1 M-bM-^@M-^S control; Group 2 M-bM-^@M-^S cells only treated with Ang II; Group 3 M-bM-^@M-^S cells pre-treated (30 minutes) with Losartan and then treated with Ang II; Group 4 M-bM-^@M-^S cells pre-treated (30 minutes) with PD123319 and then treated with Ang II. To identify which genes were significantly differentially expressed, paired t-tests (p<0.05) were performed in the following comparisons: Ang II x Control (3h); Ang II x Control (6h); Ang II +Los x Ang II (3h); Ang II +Los x Ang II (6h); Ang II +PD123319 x Ang II (3h); Ang II +PD123319 x Ang II (6h).
2014-12-20 | E-GEOD-47529 | biostudies-arrayexpress