Transcriptome analysis of inflammation-related gene expression in endothelial cells activated by complement MASP-1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE98114 | GEO | 2017/09/14
SECONDARY ACCESSION(S): PRJNA384020
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE4919: Translation State Array Analysis of Thrombin Stimulated Human Endothelial Cells GSE5352: Translation State Array Analysis of LPS Stimulated Human Endothelial Cells GSE5353: Translation State Array Analysis of Insulin Stimulated Human Endothelial Cells GSE5354: Translation State Array Analysis of TNF Stimulated Human Endothelial Cells GSE5385: Translation State Array Analysis of Histamine Stimulated Human Endothelial Cells GSE5386: Translation State Array Analysis of Serum Stimulated Human Endothelial Cells Refer to individual Series
2010-07-01 | E-GEOD-5393 | biostudies-arrayexpress
Project description:This model is from the article:
An Integrated Mathematical Model of Thrombin-, Histamine-and VEGF-Mediated Signalling in Endothelial Permeability.
Wei X, Han B, Zhang J, Liu X, Tan C, Jiang Y, Low B, Tidor B, Chen Y. BMC Syst Biol.
2011 Jul 15;5:112. 21756365
,
Abstract:
Endothelial permeability is involved in injury, inflammation, diabetes and cancer. It is partly regulated by the thrombin-, histamine-, and VEGF-mediated myosin-light-chain (MLC) activation pathways. While these pathways have been investigated, questions such as temporal effects and the dynamics of multi-mediator regulation remain to be fully studied. Mathematical modeling of these pathways facilitates such studies. Based on the published ordinary differential equation models of the pathway components, we developed an integrated model of thrombin-, histamine-, and VEGF-mediated MLC activation pathways.
RESULTS:
Our model was validated against experimental data for calcium release and thrombin-, histamine-, and VEGF-mediated MLC activation. The simulated effects of PAR-1, Rho GTPase, ROCK, VEGF and VEGFR2 over-expression on MLC activation, and the collective modulation by thrombin and histamine are consistent with experimental findings. Our model was used to predict enhanced MLC activation by CPI-17 over-expression and by synergistic action of thrombin and VEGF at low mediator levels. These may have impact in endothelial permeability and metastasis in cancer patients with blood coagulation.
CONCLUSION:
Our model was validated against a number of experimental findings and the observed synergistic effects of low concentrations of thrombin and histamine in mediating the activation of MLC. It can be used to predict the effects of altered pathway components, collective actions of multiple mediators and the potential impact to various diseases. Similar to the published models of other pathways, our model can potentially be used to identify important disease genes through sensitivity analysis of signalling components.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1102210000 | BioModels
Project description:The vascular endothelial cell (EC) monolayer plays a crucial part in maintaining hemostasis. An extensive array of G protein-coupled receptors (GPCRs) allows ECs to dynamically act on key hemostatic stimuli such as thrombin and histamine. The impact of these individual stimuli on EC signal transduction has been the subject of various studies, but insight into discordant and concordant EC signaling between different GPCRs remain limited. Using mass spectrometry- based phosphoproteomics, we delineated the unbiased signaling response for histamine stimulation in the endothelium and observed highly similar responses between different protease activated receptors (PAR1-4). Finally, we compare both histamine and PAR agonists, indicating uniquely activated proteins between both stimuli, but a general overlapping activation of cell-junction and actin cytoskeletal proteins. Thus, we provide an integrative phosphoproteomic analysis of histamine and PAR agonist in the endothelium that highlights the endothelial response programs that are at the bases of regulating hemostasis.
2024-11-27 | PXD052627 | Pride
Project description:The vascular endothelial cell (EC) monolayer plays a crucial part in maintaining hemostasis. An extensive array of G protein-coupled receptors (GPCRs) allows ECs to dynamically act on key hemostatic stimuli such as thrombin and histamine. The impact of these individual stimuli on EC signal transduction has been the subject of various studies, but insight into discordant and concordant EC signaling between different GPCRs remain limited. Using mass spectrometry- based phosphoproteomics, we delineated the unbiased signaling response for histamine stimulation in the endothelium and observed highly similar responses between different protease activated receptors (PAR1-4). Finally, we compare both histamine and PAR agonists, indicating uniquely activated proteins between both stimuli, but a general overlapping activation of cell-junction and actin cytoskeletal proteins. Thus, we provide an integrative phosphoproteomic analysis of histamine and PAR agonist in the endothelium that highlights the endothelial response programs that are at the bases of regulating hemostasis.
2024-11-27 | PXD055122 | Pride
Project description:We developed a novel substrate-selective inhibitor of p38 MAPK, UM101, and compared its effects on TNF-induced gene expression by human lung microvascular endothelial cells (HMVECLs) with the prototypical p38 catalytic inhibitor, SB203580
2017-01-10 | GSE93330 | GEO
Project description:To investigate the function of histamine signal perceived by HRH1 in the regulation of endothelial angiogenic process, we knocked down HRH1 using shRNA from histamine treated endothelial cells.
2022-08-28 | GSE211726 | GEO
Project description:This model is from the article:
Modelling thrombin generation in human ovarian follicular fluid
Bungay Sharene D., Gentry Patricia A., Gentry Rodney D.
Bulletin of Mathematical BiologyVolume 68, Issue 8, 12 July 2006, Pages 2283-302
16838084,
Abstract:
A mathematical model is constructed to study thrombin production in human ovarian follicular fluid. The model results show that the amount of thrombin that can be produced in ovarian follicular fluid is much lower than that in blood plasma, failing to reach the level required for fibrin formation, and thereby supporting the hypothesis that in follicular fluid thrombin functions to initiate cellular activities via intracellular signalling receptors. It is also concluded that the absence of the amplification pathway to thrombin production in follicular fluid is a major factor in restricting the amount of thrombin that can be produced. Titration of the initial concentrations of the various reactants in the model lead to predictions for the amount of tissue factor and phospholipid that is required to maintain thrombin production in the follicle, as well as to the conclusion that tissue factor pathway inhibitor has little effect on the time that thrombin generation is sustained. Numerical experiments to determine the effect of factor V, which is at a much reduced level in follicular fluid compared to plasma, and thrombomodulin, illustrate the importance for further experimental work to determine values for several parameters that have yet to be reported in the literature.
2024-09-02 | BIOMD0000000333 | BioModels
Project description:This model is from the article:
Modelling thrombin generation in human ovarian follicular fluid
Bungay Sharene D., Gentry Patricia A., Gentry Rodney D.
Bulletin of Mathematical BiologyVolume 68, Issue 8, 12 July 2006, Pages 2283-302
16838084,
Abstract:
A mathematical model is constructed to study thrombin production in human ovarian follicular fluid. The model results show that the amount of thrombin that can be produced in ovarian follicular fluid is much lower than that in blood plasma, failing to reach the level required for fibrin formation, and thereby supporting the hypothesis that in follicular fluid thrombin functions to initiate cellular activities via intracellular signalling receptors. It is also concluded that the absence of the amplification pathway to thrombin production in follicular fluid is a major factor in restricting the amount of thrombin that can be produced. Titration of the initial concentrations of the various reactants in the model lead to predictions for the amount of tissue factor and phospholipid that is required to maintain thrombin production in the follicle, as well as to the conclusion that tissue factor pathway inhibitor has little effect on the time that thrombin generation is sustained. Numerical experiments to determine the effect of factor V, which is at a much reduced level in follicular fluid compared to plasma, and thrombomodulin, illustrate the importance for further experimental work to determine values for several parameters that have yet to be reported in the literature.
2024-09-02 | BIOMD0000000332 | BioModels
Project description:Histamine is catalyzed by histidine decarboxylase (HDC), which plays important roles in many physiological and pathological processes, but its role in angiogenesis has not been thoroughly clarified. Here we report that HDC is highly expressed in Ly6C+macrophages, rather than in endothelial cells using Hdc-GFP transgenic mice with hindlimb ischemia (HLI) mouse model. Given the whole-process promoting effect of macrophages on angiogenesis, a cluster of HDC+CXCR2+ macrophages have been identified by single-cell sequencing technology in ischemic tissue. The inactivation of HDC leads to a lack of histamine and pro-angiogenic factor production in macrophages, inducing a harsh inflammatory microenvironment that is not conducive to the interaction between macrophages and endothelial cells. Moreover, HA-DA@histamine hydrogel has been designed and demonstrated to safely treat ischemic injury by modulating inflammation and angiogenesis. These data highlight the critical roles of HDC/histamine signaling in macrophage differentiation, angiogenesis, and muscle regeneration in the early stage of HLI.
2024-08-02 | GSE273730 | GEO
Project description:Thrombin exerts pleiotropic effects on the endothelium. Nevertheless, little is known about its capacity to generate endothelial microparticles, a hallmark of endothelial activation. To gain insight into the mechanisms involved in microparticles release, the human microvascular endothelial cell line-1 (HMEC1) was stimulated with thrombin at 1 IU/ml for different times. The gene expression profiling in stimulated HMEC-1 was compared to that obtain with untreated cells.
2006-01-20 | E-MEXP-477 | biostudies-arrayexpress