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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of rat aortic smooth muscle cells transfected with dominant negative or upregulated JNK1 and subjected to oxidative stress

ABSTRACT: Oxidative stress-dependent genes are defined as those induced or suppressed by H2O2 treatement in rat vascular smooth muscle cells. JNK-induced genes in rat vascular smooth muscle cells are defined as those induced by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and suppressed by adenovirus encoding dominant negative JNK1 (APF). JNK-suppressed genes in rat vascular smooth muscle cells are defined as those suppressed by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and induced by adenovirus encoding dominant negative JNK1 (APF). Adenovirus encoding nuclear localizing GFP was used as a control.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Hiroki Aoki

PROVIDER: E-GEOD-2190 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Regression of abdominal aortic aneurysm by inhibition of c-Jun N-terminal kinase.

Yoshimura Koichi K Aoki Hiroki H Ikeda Yasuhiro Y Fujii Kozo K Akiyama Norio N Furutani Akira A Hoshii Yoshinobu Y Tanaka Nobuyuki N Ricci Romeo R Ishihara Tokuhiro T Esato Kensuke K Hamano Kimikazu K Matsuzaki Masunori M

Nature medicine 20051127 12

Abdominal aortic aneurysm (AAA) is a common disease among elderly people that, when surgical treatment is inapplicable, results in progressive expansion and rupture of the aorta with high mortality. Although nonsurgical treatment for AAA is much awaited, few options are available because its molecular pathogenesis remains elusive. Here, we identify JNK as a proximal signaling molecule in the pathogenesis of AAA. Human AAA tissue showed a high level of phosphorylated JNK. We show that JNK program ...[more]

PMID: 16311603

Similar Datasets

JNK-dependent genes_rVSMC

Project description:Oxidative stress-dependent genes are defined as those induced or suppressed by H2O2 treatement in rat vascular smooth muscle cells. JNK-induced genes in rat vascular smooth muscle cells are defined as those induced by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and suppressed by adenovirus encoding dominant negative JNK1 (APF). JNK-suppressed genes in rat vascular smooth muscle cells are defined as those suppressed by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and induced by adenovirus encoding dominant negative JNK1 (APF). Adenovirus encoding nuclear localizing GFP was used as a control. Keywords = vascular smooth muscle Keywords = hydrogen peroxide Keywords = c-Jun N-terminal kinase Keywords = JNK Keywords = adenovirus Keywords = oxidative stress Keywords: repeat sample

2005-11-09 | GSE2190 | GEO

Phenotype modulation of VSMCs on patterned substrate

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

Transcription profiling by array of human aortic vascular smooth muscle cells treated with IL-17 or untreated

Project description:Investigate the effect of recombinant human IL-17A on vascular smooth muscle cells cultured from human aortas. Experiment Overall Design: SMCs from the aortas of three different donors were cultured in M199 media supplemented with 20% FCS and used at passage 3. The cells were either not treated or treated with IL-17 at 100 ng/ml for 6 hr. The six samples were labeled as Untreated or IL-17-treated from three independent experiments labeled A, B, and C.

2008-10-24 | E-GEOD-11367 | biostudies-arrayexpress

Angiotensin II regulated gene expression in rat primary vascular smooth muscle cells (VSMC)

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

MYOCD overexpression in HCASMs

Project description:To identify novel genes especially lncRNAs linked to vascular smooth muscle cell (VSMC) differentiation, we performed RNA sequencing of adenovirus–MYOCD transduced human coronary artery smooth muscle cells (HCASMs). Simiilar amount of empty Adenovirus was used as control.

2016-08-31 | GSE77120 | GEO

Effect of progerin on p53-deficient vascular smooth muscle cells

Project description:Analysis of p53-deficient (E6-expressing) human vascular smooth muscle cells (VSMCs) that express progerin, a mutated form of lamin A resposible for Hutchinson- Gilford progeria syndrome (HGPS). p53 pathway is associated with HGPS. Results provide insight into molecular mechanisms underlying vascular dysfunction of HGPS caused by other than p53 pathway. The gene expression of VSMCs induced to express E6 and either lamin A or progerin by retroviral vectors.

2013-09-22 | E-GEOD-47553 | biostudies-arrayexpress

Single-cell RNA-seq Reveals Unique Vascular Smooth Muscle Cell Phenotypes in Culture

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

mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC. Calcification was induced in rat aorta vascular smooth muscle cells with inorganic phosphate (Pi). Total RNA were extracted from the cells 3 and 6 days later. mRNA profile of the sample was compared with normal control.

2015-11-07 | E-GEOD-74755 | biostudies-arrayexpress

Mouse VSMC LC-MSMS - Functional and Proteomic Investigations Reveal Major Royal Jelly Protein 1 Associated with Anti-hypertension Activity in Mouse Vascular Smooth Muscle Cells

Project description:Vascular smooth muscle cells (VSMCs) are a major cell type of the arterial wall and their functionality is associated with blood pressure regulation. Although royal jelly (RJ) has reported effects on anti-hypertension, the mechanism of blood pressure regulation by major royal jelly protein 1 (MRJP1), the most abundant RJ protein, is still unknown. Therefore, mrjp1 gene was delivered into mouse VSMCs to investigate how MRJP1 influences the VSMC functionality by functional and proteomic analysis.The data here are the proteomic analysis of triplicated control and MRJP1 expressing VSMCs.

2018-10-27 | PXD004207 | Pride

Overexpression of Transcription Factor GATA6 in Human Coronary Artery Smooth Muscle Cells in vitro

Project description:Vascular smooth muscle cell plasticity plays a pivotal role in the pathophysiology of vascular diseases. Despite compelling evidence demonstrating the importance of transcription factor GATA6 in vascular smooth muscle, the functional role of GATA6 remains poorly understood. The aim of this study was to elucidate the role of GATA6 on cell migration and to gain insight into GATA6-sensitive genes in smooth muscle. Therefore, we performed Affymetrix microarray analysis on human coronary artery smooth muscle cells after overexpressing GATA6 by adenovirus transduction and compared it to control which are cell transduced with Ad-CMV-null.

2022-10-31 | GSE216686 | GEO

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