ArticleThe Journal of biological chemistry2015
Peroxiredoxin II is an antioxidant enzyme that negatively regulates collagen-stimulated platelet function.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Jak2 V617F clonal hematopoiesis promotes arterial thrombosis via platelet activation and cross talk.Blood · 2024Pooled it
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Oroxylin A reverses SHP-2 oxidative inactivation in GPVI signaling to suppress platelet activation and thrombus formation.Thrombosis journal · 2025Article
- Construction of multifunctional porcine acellular dermal matrix hydrogel blended with vancomycin for hemorrhage control, antibacterial action, and tissue repair in infected trauma wounds.Materials today. Bio · 2021Article
- Peroxiredoxins as Potential Targets for Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2021Review
- The role of redox system in metastasis formation.Angiogenesis · 2021Review
- Oxidative Stress and Preeclampsia-Associated Prothrombotic State.Antioxidants (Basel, Switzerland) · 2020Review
- Role of Peroxiredoxins in Protecting Against Cardiovascular and Related Disorders.Cardiovascular toxicology · 2020Review
- The choline transporter Slc44a2 controls platelet activation and thrombosis by regulating mitochondrial function.Nature communications · 2020Article
- ROS in Platelet Biology: Functional Aspects and Methodological Insights.International journal of molecular sciences · 2020Review
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Regulation of platelet activation and thrombus formation by reactive oxygen species.Redox biology · 2018Review
- Redox Proteomics and Platelet Activation: Understanding the Redox Proteome to Improve Platelet Quality for Transfusion.International journal of molecular sciences · 2017Review
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen-induced platelet signaling is mediated by binding to the primary receptor glycoprotein VI (GPVI). Reactive oxygen species produced in response to collagen have been found to be responsible for the propagation of GPVI signaling pathways in platelets. Therefore, it has been suggested that antioxidant enzymes could down-regulate GPVI-stimulated platelet activation. Although the antioxidant enzyme peroxiredoxin II (PrxII) has emerged as having a role in negatively regulating signaling through various receptors by eliminating H2O2 generated upon receptor stimulation, the function of PrxII in collagen-stimulated platelets is not known. We tested the hypothesis that PrxII negatively regulates collagen-stimulated platelet activation. We analyzed PrxII-deficient murine platelets. PrxII deficiency enhanced GPVI-mediated platelet activation through the defective elimination of H2O2 and the impaired protection of SH2 domain-containing tyrosine phosphatase 2 (SHP-2) against oxidative inactivation, which resulted in increased tyrosine phosphorylation of key components for the GPVI signaling cascade, including Syk, Btk, and phospholipase Cγ2. Interestingly, PrxII-mediated antioxidative protection of SHP-2 appeared to occur in the lipid rafts. PrxII-deficient platelets exhibited increased adhesion and aggregation upon collagen stimulation. Furthermore, in vivo experiments demonstrated that PrxII deficiency facilitated platelet-dependent thrombus formation in injured carotid arteries. This study reveals that PrxII functions as a protective antioxidant enzyme against collagen-stimulated platelet activation and platelet-dependent thrombosis.
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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.