ArticleJournal of thrombosis and haemostasis : JTH2014
Platelets from mice lacking the aryl hydrocarbon receptor exhibit defective collagen-dependent signaling.
Article in Journal of thrombosis and haemostasis : JTH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Aryl hydrocarbon receptor activation alters immune cell populations in the lung and bone marrow during coronavirus infection.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Uraemic solutes as therapeutic targets in CKD-associated cardiovascular disease.Nature reviews. Nephrology · 2021Review
- The Aryl Hydrocarbon Receptor in Chronic Kidney Disease: Friend or Foe?Frontiers in cell and developmental biology · 2020Review
- Review
- Indoxyl Sulfate Promotes Arterial Thrombosis in Rat Model via Increased Levels of Complex TF/VII, PAI-1, Platelet Activation as Well as Decreased Contents of SIRT1 and SIRT3.Frontiers in physiology · 2018Article
- From the Cover: Coagulation-Driven Hepatic Fibrosis Requires Protease Activated Receptor-1 (PAR-1) in a Mouse Model of TCDD-Elicited Steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Article
- Beta Hairpin Peptide Hydrogels as an Injectable Solid Vehicle for Neurotrophic Growth Factor Delivery.Biomacromolecules · 2015Article
- Breaking the mold: transcription factors in the anucleate platelet and platelet-derived microparticles.Frontiers in immunology · 2015Review
- Crosstalk of Oncogenic Signaling Pathways during Epithelial-Mesenchymal Transition.Frontiers in oncology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe previously identified aryl hydrocarbon receptor (AHR) as a novel regulator of megakaryocytic differentiation and polyploidization and reported that AHR-null mice have approximately 15% fewer platelets than do wild-type mice, yet they exhibit a dramatic, unexplained bleeding phenotype.
objectivesThe current work tests our hypothesis that AHR-null platelets are functionally deficient, contributing to the previously reported (yet unexplained) bleeding phenotype present in AHR-null mice.
methodsAHR-null bone marrow was ex vivo differentiated with thrombopoietin with or without AHR ligands or AHR inhibitors and analyzed for degree of megakaryopoiesis and polyploidization. Platelet function of AHR-null mice was assessed with aggregation and spreading assays. Platelet signaling was examined using Western analysis and Rac activity assays.
resultsAHR ligands differentiate murine bone marrow-derived progenitors into polyploid megakaryocytes in the absence of thrombopoietin, and AHR inhibitors block thrombopoietin-induced megakaryocytic differentiation. Despite their responsiveness toward thrombin, AHR-null platelets demonstrate decreased aggregation and spreading in response to collagen compared with wild-type platelets. AHR-null platelets bind fibrinogen after stimulation with thrombin or AYPGKF and aggregate in response to AYPGKF and adenosine diphosphate. Mechanistically, AHR absence led to down-regulation of Vav1 and Vav3, altered phospholipase Cγ2 phosphorylation, decreased Rac1 activation, and reduced platelet activation in response to collagen.
conclusionsThese results are consistent with a role for AHR in platelet function, especially as it relates to platelet aggregation and spreading in response to collagen. Our work suggests AHR is a critical component of the physiologic response that platelets undergo in response to collagen and may provide novel treatment options for patients with bleeding disorders.
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