ArticleBlood advances2019
Endothelial signaling by neutrophil-released oncostatin M enhances P-selectin-dependent inflammation and thrombosis.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Integrative transcriptomic analysis in human and mouse model of anaphylaxis identifies gene signatures associated with cell movement, migration and neuroinflammatory signalling.Frontiers in immunology · 2022Trial
- Neutrophil-derived oncostatin m contributes to endothelial cell dysfunction during Treponema denticola interaction.PloS one · 2026Article
- Blood perfusion through ventricular assist devices induces erythrocytes to interact with leukocytes.Biochemistry and biophysics reports · 2025Article
- Compromised efferocytosis during aging is related to COVID-19 severity in mice.Virologica Sinica · 2025Article
- Interaction Between Neutrophils and Elements of the Blood-Brain Barrier in the Context of Multiple Sclerosis and Ischemic Stroke.International journal of molecular sciences · 2025Review
- The plasma proteome reveals distinct signaling pathways associated with PR3-ANCA positive and MPO-ANCA positive vasculitis.Frontiers in immunology · 2025Article
- Dysregulated Genes and Signaling Pathways in the Formation and Rupture of Intracranial Aneurysm.Translational stroke research · 2024Article
- Communications between Neutrophil-Endothelial Interaction in Immune Defense against Bacterial Infection.Biology · 2024Review
- Progress of nanomaterials in the treatment of thrombus.Drug delivery and translational research · 2024Review
- Under the dual effect of inflammation and pulmonary fibrosis, CTD-ILD patients possess a greater susceptibility to VTE.Thrombosis journal · 2024Review
- Oncostatin M: Dual Regulator of the Skeletal and Hematopoietic Systems.Current osteoporosis reports · 2024Review
- Coagulopathy and acute pancreatitis: pathophysiology and clinical treatment.Frontiers in immunology · 2024Review
- The roles of P-selectin in cancer cachexia.Medical oncology (Northwood, London, England) · 2023Review
- Pathophysiology of deep vein thrombosis.Clinical and experimental medicine · 2023Review
- Association between higher systemic immune inflammation index (SII) and deep vein thrombosis (DVT) in patients with aneurysmal subarachnoid hemorrhage (aSAH) after endovascular treatment.Neurosurgical review · 2023Article
- Parameters to Predict the Outcome of Severe and Critical COVID-19 Patients when Admitted to the Hospital.Journal of clinical medicine · 2023Article
- Liang-Ge Decoction Ameliorates Coagulation Dysfunction in Cecal Ligation and Puncture-Induced Sepsis Model Rats through Inhibiting PAD4-Dependent Neutrophil Extracellular Trap Formation.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Pathogenesis and Therapy of Coagulation Disorders in Severe Acute Pancreatitis.Journal of inflammation research · 2023Review
- Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Inflammatory biomarkers after an exercise intervention in childhood acute lymphoblastic leukemia survivors.EJHaem · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In the earliest phase of inflammation, histamine and other agonists rapidly mobilize P-selectin to the apical membranes of endothelial cells, where it initiates rolling adhesion of flowing neutrophils. Clustering of P-selectin in clathrin-coated pits facilitates rolling. Inflammatory cytokines typically signal by regulating gene transcription over a period of hours. We found that neutrophils rolling on P-selectin secreted the cytokine oncostatin M (OSM). The released OSM triggered signals through glycoprotein 130 (gp130)-containing receptors on endothelial cells that, within minutes, further clustered P-selectin and markedly enhanced its adhesive function. Antibodies to OSM or gp130, deletion of the gene encoding OSM in hematopoietic cells, or conditional deletion of the gene encoding gp130 in endothelial cells inhibited neutrophil rolling on P-selectin in trauma-stimulated venules of the mouse cremaster muscle. In a mouse model of P-selectin-dependent deep vein thrombosis, deletion of OSM in hematopoietic cells or of gp130 in endothelial cells markedly inhibited adhesion of neutrophils and monocytes and the rate and extent of thrombus formation. Our results reveal a paracrine-signaling mechanism by which neutrophil-released OSM rapidly influences endothelial cell function during physiological and pathological inflammation.
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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.