ArticleCell death & disease2013
Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.
Article in Cell death & disease, 2013. 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, 47 citations in OpenAlex.
- Platelet Drp1 phosphorylation provides a platform for immune-based platelet function testing.Blood · 2026Article
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- Death of Leukemia Cells and Platelets Induced by 3,3'-Dihydroxy-4,5-Dimethoxybibenzyl Is Mediated by p38 Mitogen-Activated Protein Kinase Pathway.Molecules (Basel, Switzerland) · 2025Article
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- Daidzein Inhibits Human Platelet Activation by Downregulating Thromboxane AInternational journal of molecular sciences · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Thrombin Induced Apoptosis through Calcium-Mediated Activation of Cytosolic Phospholipase ABiomolecules & therapeutics · 2023Article
- Mechanisms Underlying Dichotomous Procoagulant COAT Platelet Generation-A Conceptual Review Summarizing Current Knowledge.International journal of molecular sciences · 2022Review
- Apoptosis in megakaryocytes: Safeguard and threat for thrombopoiesis.Frontiers in immunology · 2022Review
- Article
- Curcumin at Low Doses Potentiates and at High Doses Inhibits ABT-737-Induced Platelet Apoptosis.International journal of molecular sciences · 2021Article
- Renal tubular injury induced by glyphosate combined with hard water: the role of cytosolic phospholipase A2.Annals of translational medicine · 2021Article
- ASK1 inhibition triggers platelet apoptosisHaematologica · 2020Article
- Platelet Activation via Shear Stress Exposure Induces a Differing Pattern of Biomarkers of Activation versus Biochemical Agonists.Thrombosis and haemostasis · 2020Article
- Platelet microRNA-15b protects against high platelet reactivity in patients undergoing percutaneous coronary intervention through Bcl-2-mediated platelet apoptosis.Annals of translational medicine · 2020Article
- Effects of Snake-Derived Phospholipase A2 Inhibitors on Acute Pancreatitis: In vitro and in vivo Characterization.Drug design, development and therapy · 2020Article
- ABT-737 Triggers Caspase-Dependent Inhibition of Platelet Procoagulant Extracellular Vesicle Release during Apoptosis and Secondary Necrosis In Vitro.Thrombosis and haemostasis · 2019Article
- Esculetin, a Coumarin Derivative, Prevents Thrombosis: Inhibitory Signaling on PLCγ2-PKC-AKT Activation in Human Platelets.International journal of molecular sciences · 2019Article
- Down-regulation of platelet adhesion receptors is a controlling mechanism of thrombosis, while also affecting post-transfusion efficacy of stored platelets.Thrombosis journal · 2019Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influence those induced by Thr/Cvx. The inhibitor also reduced the phosphorylation of cytosolic phospholipase A2 (cPLA2), an established p38 substrate, induced by ABT-737 or Thr/Cvx. ABT-737, but not Thr/Cvx, induced the caspase 3-dependent cleavage and inactivation of cPLA2. Thus, p38 MAPK promotes ABT-737-induced apoptosis by inhibiting the cPLA2/arachidonate pathway. We also show that arachidonic acid (AA) itself and in combination with Thr/Cvx or ABT-737 at low concentrations prevented apoptotic events, whereas at high concentrations it enhanced such events. Our data support the hypothesis that the p38 MAPK-triggered arachidonate pathway serves as a defense mechanism against apoptosis under physiological conditions.
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