ArticleThrombosis and haemostasis2021
miR-204-5p and Platelet Function Regulation: Insight into a Mechanism Mediated by CDC42 and GPIIbIIIa.
Article in Thrombosis and haemostasis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- MicroRNA-223-3p is a determinant of platelet procoagulant activity.Blood advances · 2026Article
- Analysis of the expression of ARNTL2 and miR-204-5p and their correlation with clinical pathological features in NSCLC patients.American journal of clinical and experimental immunology · 2025Article
- TRIM27 revealing by tumor educated platelet RNA-sequencing, as a potential biomarker for malignant ground-glass opacities diagnosis mediates glycolysis of non-small cell lung cancer cells partially through HOXM1.Translational lung cancer research · 2024Article
- The Novel Role of Noncoding RNAs in Modulating Platelet Function: Implications in Activation and Aggregation.International journal of molecular sciences · 2023Review
- Factors Associated with Platelet Activation-Recent Pharmaceutical Approaches.International journal of molecular sciences · 2022Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSeveral platelet-derived microRNAs are associated with platelet reactivity (PR) and clinical outcome in cardiovascular patients. We previously showed an association between miR-204-5p and PR in stable cardiovascular patients, but data on functional mechanisms are lacking.
aimsTo validate miR-204-5p as a regulator of PR in platelet-like structures (PLS) derived from human megakaryocytes and to address mechanistic issues.
methodsHuman hematopoietic stem cells were differentiated into megakaryocytes, enabling the transfection of miR-204-5p and the recovery of subsequent PLS. The morphology of transfected megakaryocytes and PLS was characterized using flow cytometry and microscopy. The functional impact of miR-204-5p was assessed using a flow assay, the quantification of the activated form of the GPIIbIIIa receptor, and a fibrinogen-binding assay. Quantitative polymerase chain reaction and western blot were used to evaluate the impact of miR-204-5p on a validated target, CDC42. The impact of CDC42 modulation was investigated using a silencing strategy.
resultsmiR-204-5p transfection induced cytoskeletal changes in megakaryocytes associated with the retracted protrusion of proPLS, but it had no impact on the number of PLS released. Functional assays showed that the PLS produced by megakaryocytes transfected with miR-204-5p were more reactive than controls. This phenotype is mediated by the regulation of GPIIbIIIa expression, a key contributor in platelet-fibrinogen interaction. Similar results were obtained after CDC42 silencing, suggesting that miR-204-5p regulates PR, at least in part, via CDC42 downregulation.
conclusionWe functionally validated miR-204-5p as a regulator of the PR that occurs through CDC42 downregulation and regulation of fibrinogen receptor expression.
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