Document Type

Article

Publication Date

3-6-2025

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This article is the author's final published version in Genes, Volume 16, Issue 3, March 2025, Article number 312.

The published version is available at https://doi.org/10.3390/genes16030312.

Copyright © 2025 by the authors

Abstract

BACKGROUND: Platelets are highly enriched in microRNAs (miRNAs), which are genomically encoded 19-25 nucleotide non-coding RNAs that target complementary mRNAs through total or near-total base pairing. MiR-223 is among the most abundant miRNAs in human and murine platelets, but despite ongoing investigations in recent years, miR-223 roles in platelet physiology and its putative roles in high on-treatment platelet reactivity (HTPR) remain controversial, as studies showed varying findings.

OBJECTIVES: In the current hybrid review/report, we aim to compare studies that investigated miR-223 in platelet function and HTPR. Additionally, we briefly report our own findings on murine miR-223-deficient platelets.

METHODS: We have thoroughly searched the literature and found three studies that investigated the roles of miR-223 in platelet function by utilizing miR-223 global knockout mice, and three studies that explored the association between miR-223 and residual platelet reactivity by measuring miR-223 levels in platelets of patients treated with clopidogrel for cardiac artery disease. We assessed platelet function in response to different agonists and evaluated P2y12 levels in male and female miR-223-deficient platelets.

RESULTS: Integrin activation and α granule secretion were similar between WT and KO platelets in response to all agonists in platelets from both female and male mice, although both genotypes showed elevated thrombin response in females compared to males.

CONCLUSIONS: In all studies, including ours, taken together, miR-233 appears to play a modest role in platelet function and development of HTPR.

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This work is licensed under a Creative Commons Attribution 4.0 License.

Language

English

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