ArticleFrontiers in immunology2022
Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- The Role of Platelet-Derived Microparticles in Platelet Adhesion and Aggregation to Immobilized Extracellular Matrix Proteins Under Flow.Cellular and molecular bioengineering · 2026Article
- Novel biomarker-based prediction model for coronary artery lesions in Kawasaki disease.BMC pediatrics · 2026Article
- Platelet-derived non-coding RNAs as emerging contributors to autoimmune inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- A lipid-related transcriptomic signature for distinguishing Kawasaki disease from febrile infections: a Mendelian randomization and machine-learning study.Frontiers in immunology · 2026Article
- Effect of Platelet-Derived Microparticles on the Expression of Adhesion Molecules in Endothelial Cells.International journal of molecular sciences · 2025Article
- Amphiregulin Promotes Proliferation and Migration of the Damaged Endothelial Cells in Kawasaki Disease Cell Models.Immunity, inflammation and disease · 2025Article
- Immunophenotype of Kawasaki Disease: Insights into Pathogenesis and Treatment Response.Life (Basel, Switzerland) · 2025Review
- Platelet-Monocyte Aggregate Instigates Inflammation and Vasculopathy in Kawasaki Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-cell transcriptomic and m6A methylation analyses reveal platelet-mediated immune regulatory mechanisms in sepsis.Frontiers in immunology · 2025Article
- Age-Specific Cardiovascular and Platelet Dynamics in Kawasaki Disease.International journal of general medicine · 2025Article
- Combination of CRP and miRNA signature as a potential diagnostic strategy for Kawasaki disease.Frontiers in pediatrics · 2025Article
- miR-1915-3p regulates megakaryocytic and erythroid differentiation by targeting SOCS4.Thrombosis journal · 2024Article
- The Future of Kawasaki Disease Diagnosis: Liquid Biopsy May Hold the Key.International journal of molecular sciences · 2024Review
- MiR-223-3p affects the proliferation and apoptosis of HCAECs in Kawasaki disease by regulating the expression of FOXP3.Immunity, inflammation and disease · 2023Article
- Review
- Platelets promote CRC by activating the C5a/C5aR1 axis via PSGL-1/JNK/STAT1 signaling in tumor-associated macrophages.Theranostics · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Kawasaki disease (KD) is an acute vasculitis that may result in permanent coronary artery damage with unknown etiology. Endothelial cell (EC) dysfunction and platelet hyperactivity are the hallmarks of KD. Platelets are involved in the development of endothelial dysfunction. MiR-223 transferred by platelet microparticles (PMPs) has been found to involve in the functional regulation of endothelial cells in sepsis. However, the role of platelet-derived miR-223 in endothelial dysfunction has not yet been investigated in KD. Objectives: We seek to investigate the role of platelet-derived miR-223 in endothelial dysfunction of KD vasculopathy. Methods and results: Forty-five acute KD patients and 45 matched controls were randomly recruited in the study. When co-cultured with human coronary artery endothelial cells (HCAECs), KD platelets with higher levels of miR-223 were incorporated into HCAECs, resulting in the horizontal transfer of miR-223. Using KD platelets, PMPs, and platelet-releasate from the same amount of blood co-cultured with HCAECs, we found the increased expression of miR-223 in HCAECs was primarily derived from KD platelets, rather than PMPs or free miRNAs from platelet- releasate. KD platelet-derived miR-223 attenuated TNF-α induced intercellular cell adhesion molecule-1 (ICAM-1) expression in HCAECs. KD platelet-derived miR-223 also suppressed the monocyte adhesion to HCAECs. Conclusions: The horizontal transfer of platelet-derived miR-223 suppresses the expression of ICAM-1 in HCAECs, which at least in part attenuates leukocyte adhesion, thereby reducing endothelial damage in KD vasculitis.
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