ArticleBlood2018
Cooperative PSGL-1 and CXCR2 signaling in neutrophils promotes deep vein thrombosis in mice.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed, 103 citations in OpenAlex.
- Plasma apolipoprotein A-IV deficiency as a proteomics-identified diagnostic biomarker for heat stroke: A prospective 2-center study.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Article
- ADP-dependent platelet activation is required for thrombus formation in mice exposed to simulated flight conditions.Blood vessels, thrombosis & hemostasis · 2026Article
- Incidence and risk factors for catheter-related thrombosis in elderly patients with malignant tumors: a single-center retrospective cohort study.Frontiers in oncology · 2026Article
- Targeting p-FGFR1Biomedicines · 2025Article
- Knowledge, attitude, and practice of orthopedic, vascular surgery, and anesthesiology doctors regarding postoperative deep vein thrombosis prevention in surgical patients.Scientific reports · 2025Article
- Discrete and conserved inflammatory signatures drive thrombosis in different organs after Salmonella infection.Nature communications · 2025Article
- Targeting toll-like receptors: unveiling potential therapeutic strategies for deep vein thrombosis.Frontiers in immunology · 2025Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Neutrophil extracellular traps mediated by platelet microvesicles promote thrombosis and brain injury in acute ischemic stroke.Cell communication and signaling : CCS · 2024Article
- The role of P-selectin/PSGL-1 in regulating NETs as a novel mechanism in cerebral ischemic injury.Frontiers in neurology · 2024Review
- Article
- A thrombus is formed by a gradient of platelet activation and procoagulant endothelium.Research and practice in thrombosis and haemostasis · 2023Article
- Pathophysiology of deep vein thrombosis.Clinical and experimental medicine · 2023Review
- Review
- Low P-Selectin Glycoprotein Ligand-1 Expression in Neutrophils Associates with Disease Activity and Deregulated NET Formation in Systemic Lupus Erythematosus.International journal of molecular sciences · 2023Article
- Neutrophil extracellular traps contribute to coagulopathy after traumatic brain injury.JCI insight · 2023Article
- Pathogenesis of Anemia in Canine Babesiosis: Possible Contribution of Pro-Inflammatory Cytokines and Chemokines-A Review.Pathogens (Basel, Switzerland) · 2023Review
- Platelet-Neutrophil Crosstalk in Thrombosis.International journal of molecular sciences · 2023Review
- The role of G protein-coupled receptor in neutrophil dysfunction during sepsis-induced acute respiratory distress syndrome.Frontiers in immunology · 2023Review
- Neutrophil extracellular traps in central nervous system pathologies: A mini review.Frontiers in medicine · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation is a major contributor to deep vein thrombosis (DVT). Flow restriction of the inferior vena cava (IVC) in mice induces DVT like that in humans. In this model, P-selectin-dependent adhesion of neutrophils and monocytes leads to release of neutrophil extracellular traps (NETs) and expression of tissue factor. However, it is not known what signals cause myeloid cells to generate these procoagulant effectors. Using ultrasonography and spinning-disk intravital microscopy in genetically engineered mice, we found that engagement of P-selectin glycoprotein ligand-1 (PSGL-1) and the chemokine receptor CXCR2 on rolling neutrophils propagated signals that cooperated to induce β2 integrin-dependent arrest in flow-restricted IVCs. Unlike previous reports, PSGL-1 signaling in neutrophils did not require L-selectin, and it used tyrosine 145 rather than tyrosines 112 and 128 on the adaptor Src homology domain-containing leukocyte phosphoprotein of 76 kDa. PSGL-1 and CXCR2 signaling cooperated to increase the frequency and size of thrombi, in part by stimulating release of NETs. Unlike in neutrophils, blocking PSGL-1 or CXCR2 signaling in monocytes did not affect their recruitment into thrombi or their expression of tissue factor. Our results demonstrate that neutrophils cooperatively signal through PSGL-1 and CXCR2 to promote DVT.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.