A Novel Biological Role for von Willebrand Factor in Linking Primary Hemostasis and Innate Immunity
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ABSTRACT:
PROVIDER: PRJNA844610 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19521970_1.fastq.gz | Fastqsanger.gz | |||
| SRR19521970_2.fastq.gz | Fastqsanger.gz | |||
| SRR19521971_1.fastq.gz | Fastqsanger.gz | |||
| SRR19521971_2.fastq.gz | Fastqsanger.gz | |||
| SRR19521972_1.fastq.gz | Fastqsanger.gz |
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Project description:The plasma multimeric glycoprotein von Willebrand factor (VWF) plays a critical role in primary hemostasis by tethering platelets to exposed collagen at sites of vascular injury. Recent studies have identified additional biological roles for VWF, and in particular suggest that VWF may play an important role in regulating inflammatory responses. Critically however, the molecular mechanisms through which VWF exerts its immuno-modulatory effects remains poorly understood. In this study, we report for the first time that VWF binding to macrophages triggers direct downstream MAPkinase signaling leading to NF-kB activation and production of pro-inflammatory cytokines and chemokines. In keeping with these observations, VWF binding also promotes macrophage M1 polarization and shifts macrophage metabolism towards glycolysis in a p38 dependent manner. Cumulatively, our findings define an entirely new biological role for VWF in modulating macrophage function, and thereby establish a novel link between primary hemostasis and innate immunity.
2022-09-18 | GSE205365 | GEO
Project description:Von Willebrand factor is a paracrine/autocrine regulator of human mesenchymal stem cell adhesion to distressed/apoptotic endothelial cells. This data set examines effect of vWF on gene expression in HUVECs.
2010-11-10 | GSE19816 | GEO
Project description:Von Willebrand factor is a paracrine/autocrine regulator of human mesenchymal stem cell adhesion to distressed/apoptotic endothelial cells. This data set examines effect of vWF on gene expression in HUVECs. HUVECs were maintained in EGM2 media and treated with vWF in Hank's buffered salt solution (HBSS).
2010-11-10 | E-GEOD-19816 | biostudies-arrayexpress
Project description:Von Willebrand Factor (vWF), a plasma glycoprotein, plays essential roles in primary hemostasis, in cooperation with other coagulation factors. The glycosylation affects many biological phases during the protein life-cycle. In this work, we comprehensively characterized the microheterogeneity at all probable N-glycosites in simultaneous with O-glycosites, beside the N-occupancy estimation.An RP-LC-MS/MS system functionalized with CID and HCD tandem mass techniques was utilized. Our results showed gradual glycosylation occupancy along the protein backbone. A total of 181 glycoforms, 173 N-froms and 8 O-forms, were detected and specified into plasma vWF glycosites. Given subtle characterization of site-specific glycoforms is critical for profound understanding the protein biological functions and activity.
2022-02-23 | PXD006567 | Pride
Project description:The plasma multimeric glycoprotein von Willebrand factor (VWF) plays a critical role in primary hemostasis by tethering platelets to exposed collagen at sites of vascular injury. Recent studies have identified additional biological roles for VWF, and in particular suggest that VWF may play an important role in regulating inflammatory responses. However, the molecular mechanisms through which VWF exerts its immuno-modulatory effects remain poorly understood. In this study, we report that VWF binding to macrophages triggers downstream MAP kinase signaling, NF-κB activation and production of pro-inflammatory cytokines and chemokines. In addition, VWF binding also drives macrophage M1 polarization and shifts macrophage metabolism towards glycolysis in a p38-dependent manner. Cumulatively, our findings define an important biological role for VWF in modulating macrophage function, and thereby establish a novel link between primary hemostasis and innate immunity.
| S-EPMC9633696 | biostudies-literature
Project description:Multi-omic analysis of Von Willebrand factor regulation in endothelial colony forming cells
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Project description:Multi-omic analysis of Von Willebrand factor regulation in endothelial colony forming cells
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Project description:Arthropods include chelicerates, crustaceans, and insects that all have open circulation systems and thus require different properties of their coagulation system than vertebrates. Although the clotting reaction in the chelicerate horseshoe crab has been described in details, the overall protein composition of the resulting clot has not been analysed for any of the chelicerates. The largest class among the chelicerates is the arachnids, which includes spiders, ticks, mites, and scorpions. Here, we use a mass spectrometry-based approach to characterize the spider hemolymph clot proteome from the Brazilian whiteknee tarantula, Acanthoscurria geniculate. We focused on the insoluble part of the clot and demonstrated high concentrations of proteins homologous to the hemostasis-related and multimerization-prone von Willebrand factor. These proteins, which include hemolectins and vitellogenin homologous, were previously identified as essential components of the hemolymph clot in crustaceans and insects. Their presence in the spider hemolymph clot suggests that the origin of these proteins’ function in coagulation predates the split between chelicerates and mandibulata. The clot proteome reveals that the major proteinaceous component is the oxygen-transporting and phenoloxidase-displaying abundant hemolymph protein hemocyanin, suggesting that this protein also plays a role in clot biology. In general, many of the identified clot-proteins are related to the innate immune system, and our results support the previously suggested crosstalk between immunity and coagulation in arthropods.
2017-01-11 | PXD002500 | Pride
Project description:<p><b>Objectives:</b> Use genome-wide approaches to identify genetic variants that influence common thrombosis and hemostasis factors, as well as selected common human traits.</p> <p><b>Design/Methods:</b> The GABC study was a prospective sibling cohort design. Siblings were recruited by targeted email to the undergraduate and graduate student email lists at the University of Michigan. Healthy persons between 14 and 35 years old who had healthy siblings within the same age restriction were able to participate. Study participants agreed to an online informed consent and subsequently completed a 52-question online survey describing their specific bleeding traits as well as many common human traits. Fifty milliliters of blood was collected into a citrate-dextrose solution (ACD) from each participant. An aliquot of whole blood was used for an automated complete blood count analysis and the remainder was processed into platelet poor plasma and buffy coat portions. Plasma and buffy coat aliquots were snap frozen and stored in liquid nitrogen for future studies. 1189 individuals representing 507 sibships were collected between 06/26/2006 and 01/30/2009.</p> <p><b>Phenotyping Survey Details:</b> To characterize individual bruising and bleeding history, the online survey recorded answers to questions based on a modified von Willebrand Disease (VWD) screening questionnaire. To characterize a collection of participant's common human traits, the survey recorded answers to questions about height, weight, presence of skin tags, history of acne, eye color, hair color, hair line characteristics, skin sunburn sensitivity, skin tanning ability, natural skin color, freckling, cheek dimpling, earlobe shape, shoe size, foot arch characteristics, hand fifth digit morphology, history of dyslexia, history of migraine headaches, history of seasonal allergies, history of apthous ulcers, tendency to sneeze while walking into a bright sunny place, history of dental caries, need for corrective eye lenses, handedness and like or dislike of strongly flavored foods. <b>Biochemical phenotyping:</b> Assays for plasma Von Willebrand Factor (VWF) antigen were performed using ELISA and "Alphalisa" techniques. Automated complete blood count analysis was performed on a Bayer Advia 120 on all participants (including WBC differential, RBC indices, and platelet count.) For the dbGaP v2 update, new biochemical phenotypes have been submitted and include von Willebrand Factor, von Willebrand Factor propeptide, plasminogen, gamma prime fibrinogen, ADAMTS 13, antithrombin III, protein C, and protein S. All new phenotypes were obtained using "Alphalisa" techniques. <b>Genotyping Details:</b> SNP genotyping was performed using genomic DNA extracted from peripheral blood at the Broad Institute, (MIT/Harvard). Genotyping was performed on the Illumina Omni-1 quad chip at the Broad Institute. For the dbGaP v2 update, genotyping data from the Illumina Human Exome was deposited.</p> <p>This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to blood clotting through large-scale genome-wide association studies of siblings. Genotyping was performed at the Broad Institute of MIT and Harvard, a GENEVA genotyping center. Data cleaning and harmonization was performed by the primary investigators at the University of Michigan, Ann Arbor, and at the GEI-funded GENEVA Coordinating Center at the University of Washington.</p> <p>This study serves as a resource for investigators who are interested in the genetic determinants of specific plasma proteins in a healthy population. The sibling cohort design allows for linkage analysis in addition to association studies. Analysis of thrombosis and hemostasis related traits should help elucidate specific biochemical and genetic networks that maintain hemostasis. We hope to identify specific genetic determinants of VWF levels in order to better understand the factors that influence the development of VWD.</p>
| phs000304 | dbGaP
Project description:Linking Indirect Effects of Cytomegalovirus to Modulation of Monocyte Innate Immune Function
| PRJNA545723 | ENA