ArticleArteriosclerosis, thrombosis, and vascular biology2014
Platelet glycoprotein Ib-IX as a regulator of systemic inflammation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Diminished plasma levels of GPIb-Frontiers in medicine · 2026Trial
- Platelet glycoprotein VI modulates leukocyte characteristics in sepsis-induced systemic inflammatory response in male mice.Physiological reports · 2026Article
- Dynamic thrombocytopenia following cardiac arrest is associated with systemic inflammation and predicts increased mortality.BMC emergency medicine · 2026Article
- A Boolean Seven-Layer Platelet Decision Model Models Consistently the Logic and Semiquantitatively the Dynamics of Platelet Activation and Inhibition.Computational and structural biotechnology journal · 2026Article
- Platelets Modulate Leukocyte Population Composition Within Perivascular Adipose Tissue.International journal of molecular sciences · 2025Article
- Platelet Glycoprotein Ibα Cytoplasmic Tail Exacerbates Thrombosis During Bacterial Sepsis.International journal of molecular sciences · 2024Article
- Platelets, inflammation, and purinergic receptors in chronic kidney disease.Kidney international · 2024Review
- The Function of ASK1 in Sepsis and Stress-Induced Disorders.International journal of molecular sciences · 2023Review
- Platelets at the Crossroads of Pro-Inflammatory and Resolution Pathways during Inflammation.Cells · 2022Review
- Fast clearance of platelets in a commonly used mouse model for GPIbα is impeded by an anti-GPIbβ antibody derivative.Journal of thrombosis and haemostasis : JTH · 2022Article
- Platelet glycoprotein Ibα provides radiation protection.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2022Article
- Platelet Glycoprotein Ib α-Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- The dual role of platelet-innate immune cell interactions in thrombo-inflammation.Research and practice in thrombosis and haemostasis · 2020Review
- Thrombocytopenia Impairs Host Defense Against Burkholderia pseudomallei (Melioidosis).The Journal of infectious diseases · 2019Article
- Platelets modulate multiple markers of neutrophil function in response to in vitro Toll-like receptor stimulation.PloS one · 2019Article
- Platelets in Sepsis: An Update on Experimental Models and Clinical Data.Frontiers in immunology · 2019Review
- Measuring and interpreting platelet-leukocyte aggregates.Platelets · 2018Review
- Do platelets promote cardiac recovery after myocardial infarction: roles beyond occlusive ischemic damage.American journal of physiology. Heart and circulatory physiology · 2018Article
- Translational Implications of Platelets as Vascular First Responders.Circulation research · 2018Review
- Platelets regulate leucocyte responses to Toll-like receptor stimulation.Clinical & translational immunology · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe platelet glycoprotein Ib-IX (GP Ib-IX) receptor is a well-characterized adhesion receptor supporting hemostasis and thrombosis via interactions with von Willebrand factor. We examine the GP Ib-IX/von Willebrand factor axis in murine polymicrobial sepsis, as modeled by cecal ligation and puncture (CLP). APPROACH AND
resultsGenetic absence of the GP Ib-IX ligand, von Willebrand factor, prolongs survival after CLP, but absence of the receptor, GP Ib-IX, does not. Because absence of either von Willebrand factor or GP Ib-IX significantly impairs hemostasis and thrombosis, we sought to define additional GP Ib-IX-dependent pathways impacting survival in the CLP model. We document that the absence of GP Ib-IX leads to reduced platelet-neutrophil and platelet-monocyte interactions. Twenty-four hours after CLP, absence of GP Ib-IX coincides with an alteration in cytokine levels, such as tumor necrosis factor-α secreted by monocytes, and increased macrophage-1 antigen expression by neutrophils.
conclusionsIn contrast to the well-characterized proinflammatory properties of platelets, we describe in the CLP model an anti-inflammatory property associated with platelet GP Ib-IX. Thus, a single platelet receptor displays a dual modulatory role in both the thrombotic and inflammatory pathways associated with polymicrobial sepsis. In sharing leucine-rich motifs with toll-like receptors, platelet GP Ib-IX can be considered a multifunctional participant in hemostasis, thrombosis, and the inflammatory cascade. The results highlight a dynamic role for platelets in systemic inflammation and add to the complex pathophysiologic events that occur during the dysregulated coagulation and inflammation associated with sepsis.
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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.