Publications by authors named "Virginie Gourdou-Latyszenok"
Article Synopsis
- Venous thromboembolism is linked to endothelial cell activation, inflammation, and the release of extracellular RNA (eRNA), with TLR3 potentially serving as the receptor for eRNA in this process.
- Experiments involving mice with and without TLR3 showed that eRNA influenced thrombus size and formation, with treatments affecting signaling pathways and neutrophil recruitment.
- Overall, the study highlights the role of TLR3 and eRNA in promoting venous thromboembolism, indicating their potential as therapeutic targets for managing this condition.
Article Synopsis
- Neutrophils contribute to thrombosis by forming extracellular traps (NETs), and this process is observed in patients with myeloproliferative neoplasms (MPNs) with the JAK2V617F mutation.
- The study explores if JAK2V617F neutrophils alone can cause thrombosis, and findings reveal that they need cooperation from mutated platelets to promote NETosis and subsequent thrombosis.
- Additionally, aspirin treatment was shown to reduce NET formation and lung thrombosis in mouse models and lower NET marker levels in MPN patients treated with aspirin, highlighting its potential role in preventing thrombosis.
Reduced blood flow velocity in the vein triggers inflammation and is associated with the release into the extracellular space of alarmins or damage-associated molecular patterns (DAMPs). These molecules include extracellular nucleic acids, extracellular purinergic nucleotides (ATP, ADP), cytokines and extracellular HMGB1. They are recognized as a danger signal by immune cells, platelets and endothelial cells.
View Article and Find Full Text PDFThe major weakness of most knock-in JAK2V617F mouse models is the presence of the JAK2 mutation in all rather than in a few hematopoietic stem cells (HSC), such as in human "early-stage" myeloproliferative neoplasms (MPN). Understanding the mechanisms of disease initiation is critical as underscored by the incidence of clonal hematopoiesis of indeterminate potential associated with JAK2V617F. Currently, such studies require competitive transplantation.
View Article and Find Full Text PDFEssentials To reliably study the respective roles of blood and endothelial cells in hemostasis, mouse models with a strong and specific endothelial expression of the Cre recombinase are needed. Using mT/mG reporter mice and conditional JAK2 mice, we compared Pdgfb-iCreERT2 and Cdh5(PAC)-CreERT2 with well-characterized Tie2-Cre mice. Comparison of recombination efficiency and specificity towards blood lineage reveals major differences between endothelial transgenic mice.
View Article and Find Full Text PDFThrombosis is the main cause of morbidity and mortality in patients with JAK2 myeloproliferative neoplasms. Recent studies have reported the presence of JAK2 in endothelial cells of some patients with myeloproliferative neoplasms. We investigated the role of endothelial cells that express JAK2 in thrombus formation using an model of human endothelial cells overexpressing JAK2 and an model of mice with endothelial-specific JAK2 expression.
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