ABSTRACT NUMBER: ESOC2026YS217 MECHANISM STUDY ON PLATELET MIR-200A-3P ABNORMALITY AND ENDOTHELIAL CELL DYSFUNCTION MEDIATED BY ACUTE ISCHEMIC STR

Abstract Background and aims Background and Objective: To investigate the expression changes of miR-200a-3p in platelets of patients with acute ischemic stroke (AIS) and its mechanism of regulating endothelial cell function through platelet-derived microvesicles (PMVs). Methods qRT-PCR was used to analyze the expression of miR-200a-3p, and logistic regression, ROC curve, and clinical scores (NIHSS, mRs) were combined to analyze correlations. Bioinformatics was applied to predict target genes and enrich pathway analysis. Dual-luciferase assays, cell transfection, and co-culture experiments were used to verify the targeting relationship, PMV-mediated transfer process, and effects on endothelial cell function. Results miR-200a-3p was highly expressed in platelets of AIS patients and was an independent risk factor for disease onset. Target genes were enriched in the atherosclerosis pathway, with MAPK14 as a core gene regulating ET-1 and VEGFA. PMVs (150 nm, positive for CD9/CD63/TSG101) transferred miR-200a-3p to endothelial cells, downregulating MAPK14 and upregulating ET-1/VEGFA. miR-200a-3p promoted endothelial cell proliferation, apoptosis, and vascular network formation. Conclusion: Platelet miR-200a-3p participates in the pathological process of AIS by targeting and inhibiting the MAPK14/c-Jun pathway through PMVs, providing a new target for diagnosis and treatment. Conflict of interest Huangwenyi nothing to disclose