ArticlePloS one2015
Vascular Smooth Muscle Cells Stimulate Platelets and Facilitate Thrombus Formation through Platelet CLEC-2: Implications in Atherothrombosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
- C-type lectin-like receptor 2 in platelets amplifies inflammation in rheumatoid arthritis.Research and practice in thrombosis and haemostasis · 2025Article
- The Dectin-1 and Dectin-2 clusters: C-type lectin receptors with fundamental roles in immunity.EMBO reports · 2024Review
- Platelets in Thrombosis and Atherosclerosis: A Double-Edged Sword.The American journal of pathology · 2024Review
- C-type lectin-like receptor 2: roles and drug target.Thrombosis journal · 2024Review
- Platelet biology and function: plaque erosion vs. rupture.European heart journal · 2024Review
- Inhibition of cancer cell‑platelet adhesion as a promising therapeutic target for preventing peritoneal dissemination of gastric cancer.Oncology letters · 2023Article
- Platelet functional abnormalities in pediatric patients with kaposiform hemangioendothelioma/Kasabach-Merritt phenomenon.Blood advances · 2023Article
- Podoplanin: A potential therapeutic target for thrombotic diseases.Frontiers in neurology · 2023Review
- Platelet and Megakaryocyte Roles in Innate and Adaptive Immunity.Circulation research · 2022Review
- Minimally Oxidized-LDL-Driven Alterations in the Level of Pathological Mediators and Biological Processes in Carotid Atherosclerosis.Cardiology and cardiovascular medicine · 2022Article
- Bench-to-Bedside in Vascular Medicine: Optimizing the Translational Pipeline for Patients With Peripheral Artery Disease.Circulation research · 2021Review
- Development of anti-thrombotic vaccine against human S100A9 in rhesus monkey.Scientific reports · 2021Article
- Heme activates platelets and exacerbates rhabdomyolysis-induced acute kidney injury via CLEC-2 and GPVI/FcRγ.Blood advances · 2021Article
- CLEC-2 Prevents Accumulation and Retention of Inflammatory Macrophages During Murine Peritonitis.Frontiers in immunology · 2021Article
- The Role of CLEC-2 and Its Ligands in Thromboinflammation.Frontiers in immunology · 2021Review
- Control of Platelet CLEC-2-Mediated Activation by Receptor Clustering and Tyrosine Kinase Signaling.Biophysical journal · 2020Article
- Pathophysiology of atherothrombosis: Mechanisms of thrombus formation on disrupted atherosclerotic plaques.Pathology international · 2020Review
- Plasma soluble C-type lectin-like receptor-2 is associated with the risk of coronary artery disease.Frontiers of medicine · 2020Article
- Transcriptomic profiling of experimental arterial injury reveals new mechanisms and temporal dynamics in vascular healing response.JVS-vascular science · 2020Article
- Podoplanin regulates the migration of mesenchymal stromal cells and their interaction with platelets.Journal of cell science · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The platelet receptor CLEC-2 is involved in thrombosis/hemostasis, but its ligand, podoplanin, is expressed only in advanced atherosclerotic lesions. We investigated CLEC-2 ligands in vessel walls. Recombinant CLEC-2 bound to early atherosclerotic lesions and normal arterial walls, co-localizing with vascular smooth muscle cells (VSMCs). Flow cytometry and immunocytochemistry showed that recombinant CLEC-2, but not an anti-podoplanin antibody, bound to VSMCs, suggesting that CLEC-2 ligands other than podoplanin are present in VSMCs. VSMCs stimulated platelet granule release and supported thrombus formation under flow, dependent on CLEC-2. The time to occlusion in a FeCl3-induced animal thrombosis model was significantly prolonged in the absence of CLEC-2. Because the internal elastic lamina was lacerated in our FeCl3-induced model, we assume that the interaction between CLEC-2 and its ligands in VSMCs induces thrombus formation. Protein arrays and Biacore analysis were used to identify S100A13 as a CLEC-2 ligand in VSMCs. However, S100A13 is not responsible for the above-described VSMC-induced platelet activation, because S100A13 is not expressed on the surface of normal VSMCs. S100A13 was released upon oxidative stress and expressed in the luminal area of atherosclerotic lesions. Suspended S100A13 did not activate platelets, but immobilized S100A13 significantly increased thrombus formation on collagen-coated surfaces. Taken together, we proposed that VSMCs stimulate platelets through CLEC-2, possibly leading to thrombus formation after plaque erosion and stent implantation, where VSMCs are exposed to blood flow. Furthermore, we identified S100A13 as one of the ligands on VSMCs.
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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.