Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389573 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5656190.fastq.gz | Fastqsanger.gz | |||
| SRR5656191.fastq.gz | Fastqsanger.gz | |||
| SRR5656192.fastq.gz | Fastqsanger.gz | |||
| SRR5656183.fastq.gz | Fastqsanger.gz | |||
| SRR5656193.fastq.gz | Fastqsanger.gz |
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Project description:G protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the β-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways
2017-09-05 | GSE99770 | GEO
Project description:The strength and duration of extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation can define the phenotypic outcome of cells. Stimualtion of the proteinase-activated receptor (Par) triggers a Gi-dependent long-lasting transactivation of the epidermal growth factor receptor and subsequent ERK1/2 phosphorylation. To understand the mechnaisms underlying this signaling cascade, microarray analysis was performed in vascular smooth muscle cells. Experiment Overall Design: Par receptors on neonatal rat aortic smooth muscle cells were stimulated with thrombin or TRAP in presence or abscence of Gi-uncoupling pertussis toxin.
2009-05-02 | E-GEOD-15841 | biostudies-arrayexpress
Project description:The strength and duration of extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation can define the phenotypic outcome of cells. Stimualtion of the proteinase-activated receptor (Par) triggers a Gi-dependent long-lasting transactivation of the epidermal growth factor receptor and subsequent ERK1/2 phosphorylation. To understand the mechnaisms underlying this signaling cascade, microarray analysis was performed in vascular smooth muscle cells.
2009-04-28 | GSE15841 | GEO
Project description:Platelet-derived growth factor (PDGF) signalling and the subsequent activation of the calcium ion channel, ORAI1 are critical drivers of pathological remodelling of native vascular smooth muscle cells to proliferative state, which is a process associated with various vascular diseases. This study aims to reveal transcriptional networks altered following ORAI1 inhibition in vascular smooth muscle cells. To study the effect of ORAI1 inhibition on VSMC biology, we performed RNA-Seq analysis of PDGF-stimulated primary human aortic smooth muscle cells treated with either ORAI1 inhibitor, (n=4) or with vehicle (n=4), and investigated the effect of ORAI1 inhibition on the transcriptional response of cells.
2023-09-21 | E-MTAB-10955 | biostudies-arrayexpress
Project description:This model is from the article:
Competing G protein-coupled receptor kinases balance G protein and β-arrestin signaling
Heitzler D, Durand G, Gallay N, Rizk A, Ahn S, Kim J, Violin JD, Dupuy L, Gauthier C, Piketty V, Crépieux P, Poupon A, Clément F, Fages F, Lefkowitz RJ, Reiter E. Mol Syst Biol.
2012; 8: 590. 22735336
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Abstract:
Seven-transmembrane receptors (7TMRs) are involved in nearly all aspects of chemical communications and represent major drug targets. 7TMRs transmit their signals not only via heterotrimeric G proteins but also through β-arrestins, whose recruitment to the activated receptor is regulated by G protein-coupled receptor kinases (GRKs). In this paper, we combined experimental approaches with computational modeling to decipher the molecular mechanisms as well as the hidden dynamics governing extracellular signal-regulated kinase (ERK) activation by the angiotensin II type 1A receptor (AT(1A)R) in human embryonic kidney (HEK)293 cells. We built an abstracted ordinary differential equations (ODE)-based model that captured the available knowledge and experimental data. We inferred the unknown parameters by simultaneously fitting experimental data generated in both control and perturbed conditions. We demonstrate that, in addition to its well-established function in the desensitization of G-protein activation, GRK2 exerts a strong negative effect on β-arrestin-dependent signaling through its competition with GRK5 and 6 for receptor phosphorylation. Importantly, we experimentally confirmed the validity of this novel GRK2-dependent mechanism in both primary vascular smooth muscle cells naturally expressing the AT(1A)R, and HEK293 cells expressing other 7TMRs.
2024-09-02 | BIOMD0000000842 | BioModels
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
Project description:The proper response to shear stress involves multiple cell components of the vascular wall including endothelial cells (ECs), smooth muscle cells (SMCs), and the intercellular communications between them. Mounting evidence indicates that retinoid acid receptor-related orphan receptor-α (RORα) mediates many biological activities of melatonin including transactivation of transcriptional factors, and anti-inflammation. In this study we investigated the effect of melatonin on endothelial cells-derived exosomal miRNA expression. We used microarrays to detail the global program of gene expression underlying melatonin treatment and identified distinct classes of dys-regulated genes during this process.
2020-10-20 | GSE159641 | GEO
Project description:Canonical Wnt/β-catenin signalling is an essential regulator of various cellular functions throughout development and adulthood. Aberrant Wnt/β-catenin signalling also contributes to various pathologies including cancer, necessitating an understanding of cell context dependent mechanisms regulating this pathway. Since protein-protein interactions underpin β-catenin function and localization, we sought to identify novel β-catenin interacting partners by affinity purification coupled with tandem mass spectrometry in vascular smooth muscle cells (VSMCs), where β-catenin is involved in both physiological and pathological control of cell proliferation. Here, we report novel components of the VSMC β-catenin interactome.
2018-10-25 | PXD010421 | Pride
Project description:Smooth muscle cells (SMCs) are important in a number of physiological systems and organs, including the cardiovascular system. The hallmark property of differentiated SMCs is the ability to contract, but contractile SMCs themselves show a range of phenotypes allowing prolonged tonic contraction in vascular smooth muscle or rapid phasic contraction in tissues such as bladder. Another distinctive characteristic, in contrast with terminally differentiated striated muscle cells, is that SMCs exhibit phenotypic plasticity. Vascular SMCs are able to modulate their phenotype along a continuum between a contractile phenotype, characteristic of healthy blood vessels, and a more proliferative âsyntheticâ phenotype, so-named for the enhanced synthesis and secretion of extracellular matrix components. Synthetic phenotype cells are found in a number of pathological situations such as atherosclerosis and arterial injury. We used mouse exon-junction (MJAY) arrays to gain insights into both the global contribution of alternative splicing events in re-shaping the transcriptome of dedifferentiating mouse aorta and bladder SMCs, and into the underlying regulatory mechanisms of the alternative splicing program. Affymetrix splice junction arrays (MJAY) were used to profile changes in both alternative splicing and transcript levels during the phenotypic modulation of smooth muscle cells when placed in culture. RNA extracted from intact aorta and bladder smooth muscle tissue was used for differentiated samples. For dedifferentiated, proliferative samples smooth muscle cells were enzymatically dispersed and grown in tissue culture for a week. Triplicate RNA samples were prepared from smooth muscle tissue of mouse aorta and bladder (differentiated) and from smooth muscle cells from each tissue cultured for 7 days (proliferative). The samples allowed comparison of alternative splicing (and other transcriptome) changes between differentiated and proliferative smooth muscle cell samples from two distinct types of smooth muscle cell, as well as allowing direct comparison of aorta (tonic smooth muscle) and bladder (phasic smooth muscle).
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Project description:BMPR2 mutation is the cause of most hereditary pulmonary arterial hypertension, but the common molecular consequence of different types of BMPR2 mutation is still not known. The goal of this study was to determine the common molecular consequences of three different classes of patient-derived BMPR2 mutation in vascular smooth muscle gene expression. Three different classes of BMPR2 mutation, wild-type BMPR2, or empty vector were stably transfected into A7R5 vascular smooth muscle cells, and expression compared.
2010-08-25 | E-GEOD-21573 | biostudies-arrayexpress