ArticleBiomedicines2021
Essential Role of Rho-Associated Kinase in ABO Immune Complex-Mediated Endothelial Barrier Disruption.
Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Major ABO-Incompatible Platelet Transfusions Are Associated With Brain Ischemia After Intracerebral Hemorrhage.Stroke · 2025Article
- A novel polypeptide from stony coral Goniopora columna inhibits thrombosis by interfering with the contact-kinin pathway.Archives of toxicology · 2025Article
- Differences in outcomes associated with ABO blood groups in recipients of IVIG.Blood vessels, thrombosis & hemostasis · 2025Article
- P-Selectin, Vascular Endothelial Cadherin, and Vascular Cell Adhesion Molecule-1 as Novel Biomarkers for ABO Hemolytic Disease of the Fetus and Newborn.Analytical cellular pathology (Amsterdam) · 2025Article
- ABO blood group, ABO mismatched transfusions and leukoreduction of transfusions in hemostatic resuscitation studies.Frontiers in bioengineering and biotechnology · 2024Article
- Associations between ABO non-identical platelet transfusions and patient outcomes-A multicenter retrospective analysis.Transfusion · 2023Article
- ABO blood group antigens and differential glycan expression: Perspective on the evolution of common human enzyme deficiencies.iScience · 2023Review
- ABO blood groups and galectins: Implications in transfusion medicine and innate immunity.Seminars in immunologyReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
ABO immune complexes (ABO-IC) formed by ABO-incompatible antigen-antibody interaction are associated with hemolysis and platelet destruction in patients transfused with ABO-nonidentical blood products. However, the effects of ABO-IC on endothelial cells (EC) are unclear. ABO-IC were formed in vitro from normal donor-derived plasma and serum. Human pulmonary artery EC (HPAEC) were cultured and treated with media, ABO-identical and -non-identical plasma, and ABO-IC. EC barrier integrity was evaluated using transendothelial electrical resistance (TEER), scanning electron microscopy (SEM), vascular endothelial (VE)-cadherin and phalloidin staining, and Rho-associated Kinase (ROCK) inhibitor treatment. TEER revealed significant/irreversible barrier disruption within 1-2 h of exposure to ABO non-identical plasma and ABO-IC; this occurred independently of EC ABO type. Treatment with ABO-IC resulted in decreased VE-cadherin staining and increased phalloidin staining in a time-dependent manner, suggesting that the resultant increased EC barrier permeability is secondary to actin stress fiber formation and loss of cell surface VE-cadherin. Inhibition of ROCK was effective in protecting against IC-induced barrier disruption even two hours after ABO-IC exposure. ABO-IC causes increased EC barrier permeability by decreasing cell surface VE-cadherin and promoting stress fiber formation, which is preventable by inhibiting ROCK activation to protect against EC contraction and gap formation.
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Registered trials
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