Gene expression profiling using microarray in rat aortic vascular smooth muscle cells in response to Angiotensin II stimulation
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Szilvia Barsi
PROVIDER: E-MTAB-14626 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Constitutively activated JNK is associated with HTLV-1 mediated tumorigenesis.
Xu X X Heidenreich O O Kitajima I I McGuire K K Li Q Q Su B B Nerenberg M M
Oncogene 19960701 1
Human T cell leukemia virus type I (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL) and HTLV-1 associated myelopathy, also called tropical spastic paraparesis (HAM/TSP). Both clinical and in vitro evidence have demonstrated that the virus or its transactivator Tax, are transforming. However, transformation appears to require additional, as yet poorly characterized, genetic changes in infected cells. JNK is a recently characterized member of the MAP kinase family. Its signaling casc ...[more]
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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:Atherosclerosis is one of the causative factors leading to the development of cardiovascular disease. Angiotensin II (AngII) is implicated in the pathological processes underlying atherosclerosis. We investigated the AngII regulated gene expression in primary vascular smooth muscle cells (VSMC). VSMCs were isolated from the thoracic aorta of male Wistar rats. Serum deprived VSMCs were stimulated with 100 nM AngII or vehicle for 2 hours, then RNA-Sequencing was carried out.
2022-07-03 | E-MTAB-11863 | 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:Acute aortic dissection (AAD) is one of the major aortic diseases that occurs without a preceding symptom and often results in sudden death. Despite the recent advances in cardiovascular medicine, AAD remains a serious problem because its molecular pathogenesis is largely unknown. In this paper, we report our serendipitous discovery that stress-induced expression of tenascin C (TNC), a member of matricellular proteins, is the protection mechanism of aorta to prevent AAD. The aortic wall stress imposed by the aortic stiffening and the angiotensin II infusion caused the strong induction of TNC in wild type mouse aorta without gross morphological changes. While TNC knockout mice at the baseline showed no morphological, histological or biomechanical abnormalities of aorta, deletion of TNC gene rendered the aorta susceptible to AAD upon the aortic stress. The stressed TNC-null aorta showed the loss of the tensile strength due to the insufficient expression of extracellular matrix proteins and the exaggerated proinflammatory response before the onset of AAD. Therefore, TNC works as a stress-activated molecular damper both by reinforcing the tensile strength and by limiting the excessive proinflammatory response in aorta. Thus far, the molecular event that leads to the AAD development has been unclear because of the unpredictable nature of the AAD onset. This study sheds light on the previously unrecognized tissue protection mechanism that converts the potentially harmful stress response into the active reinforcement of the aorta, of which failure leads to the development of AAD. Although TNC is expressed in various tissues upon the mechanical and proinflammatory stimuli, its role has long been a mystery. Our data uncovered the adaptive role of TNC in aorta that must be resilient to the continuous hemodynamic and humoral stress for lifetime. We used periaortic application of 0.5 M CaCl2 to the infrarenal aorta or either wild type (WT) or tenascin C knockout (TNC-KO) mice to create the mouse model for stiffened aorta and infused the mice with AngII (1 µg/min/kg) for 1 week to apply the pathological stress on aorta (Ca+AngII). Mice were then killed with an overdose of pentobarbital to obtain the tissue samples. The suprarenal aortic samples, from the level of right renal artery to 10 mm above the right renal artery, and infrarenal aortic samples, from the level of left renal artery to 10 mm below the left renal artery, were collected and kept in RNAlater (Qiagen) until the extraction of total RNA using RNeasy (Qiagen). We obtained the RNA samples from 8 mice with Ca+AngII treatment and 5 mice without Ca+AngII treatment for each genotype. We pooled the RNA samples with the identical experimental condition to perform the transcriptome analysis using Mouse Genome 430 2.0 (Affymetrix). We obtained suprarenal aortic smooth muscle cells (ASMCs) from TNC-KO mice by enzymatic dispersion and cultured them in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum. We cultured TNC-KO ASMCs in the presence or absence of exogenous TNC (10 µg/mL) and stimulated the cells with 10 ng/mL TNF-alpha for 24 h before obtaining total RNA using RNeasy. We used 3 independent ASMC cultures without the exogenous TNC and 4 independent cultures with the exogenous TNC. We hybridized each of the RNA samples individually to Mouse Genome 430 2.0 Array (Affymetrix).
2015-03-27 | E-GEOD-36899 | 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.
2013-06-30 | GSE38056 | GEO
Project description:Vascular smooth muscle cells (vSMC) exert a critical role in sensing and maintaining vascular integrity. These cells abundantly express the low-density lipoprotein receptor-related protein 1 (LRP1), a large endocytic and signaling receptor that recognizes numerous ligands including ApoE-rich lipoproteins, proteases, and protease-inhibitor complexes. We observed the spontaneous formation of aneurysms in the superior mesenteric artery (SMA) of both male and female mice in which LRP1 was genetically deleted in v SMC (smLRP1-/- mice). Quantitative proteomics revealed elevated abundance of several proteins in smLRP1-/- mice that are known to be induced by angiotensin II (AngII)-mediated signaling, suggesting that this pathway is dysregulated. Administration of losartan, an AngII type I receptor antagonist, or an angiotensinogen antisense oligonucleotide to reduce plasma angiotensinogen concentrations restored the normal SMA phenotype in smLRP1-/- mice and prevented aneurysm formation. Additionally, employing a vascular injury model, we noted excessive vascular remodeling and neointima formation in smLRP1-/- mice that was restored by losartan administration. Together, these findings reveal that LRP1 regulates vascular integrity and remodeling of the SMA by attenuating excessive AngII-mediated signaling.
2023-03-11 | PXD038236 | Pride
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.
2010-11-01 | E-GEOD-24932 | 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:Background. Heterogeneity in vascular smooth muscle cells (VSMCs) has been classically defined with a small set of predefined markers. Single cell genomics provides a unique unbiased approach to evaluate VSMC phenotypes. Objectives. The goal of this study was to define the heterogeneity of primary murine VSMCs grown in culture. VSMCs grown in culture are routinely used as a model of VSMCs in the vessel wall. We wanted to better understand the assumptions of this model. RNA sequencing was performed on single aortic VSMCs from 3-4 month old male mice at passages 1 and 2 (P1 and P2). Single cell contractility measurements were performed using Traction Force microscopy.
2016-03-22 | E-GEOD-79436 | biostudies-arrayexpress
Project description:Loss of contractility and acquisition of an epithelial phenotype of vascular smooth muscle cells (VSMCs) are key events in proliferative vascular pathologies such as atherosclerosis and post-angioplastic restenosis. There is no proper cell culture system allowing VSMC differentiation so that it is difficult to delineate the molecular mechanism responsible for proliferative vasculopathy. We investigated whether a micro-patterned substrate could restore the contractile phenotype of VSMCs in vitro. To induce and maintain the differentiated VSMC phenotype in vitro, we introduced a micro-patterned groove substrate to modulate the morphology and function of VSMCs.
2013-11-14 | E-MTAB-1888 | biostudies-arrayexpress