Askari Shayan, Goldfinger Lawrence E
Cardeza Foundation for Hematologic Research, Department of Medicine, Division of Hematology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Genes (Basel). 2025 Mar 6;16(3):312. doi: 10.3390/genes16030312.
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.
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.
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.
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.
In all studies, including ours, taken together, miR-233 appears to play a modest role in platelet function and development of HTPR.
血小板中富含微小RNA（miRNA），这些微小RNA是基因组编码的19 - 25个核苷酸的非编码RNA，通过完全或近乎完全的碱基配对靶向互补mRNA。MiR - 223是人和小鼠血小板中最丰富的miRNA之一，但尽管近年来一直在进行研究，miR - 223在血小板生理学中的作用及其在治疗中高血小板反应性（HTPR）中的假定作用仍存在争议，因为研究结果各不相同。
在当前的综述/报告中，我们旨在比较研究miR - 223在血小板功能和HTPR方面的研究。此外，我们简要报告我们自己关于小鼠miR - 223缺陷血小板的研究结果。
我们全面检索了文献，发现三项研究通过利用miR - 223全基因敲除小鼠研究了miR - 223在血小板功能中的作用，以及三项研究通过测量接受氯吡格雷治疗冠心病患者血小板中的miR - 223水平来探索miR - 223与残余血小板反应性之间的关联。我们评估了对不同激动剂的血小板功能，并评估了雄性和雌性miR - 223缺陷血小板中的P2y12水平。
雌性和雄性小鼠血小板中，野生型（WT）和敲除型（KO）血小板对所有激动剂的整合素激活和α颗粒分泌相似，尽管两种基因型在雌性中对凝血酶的反应均高于雄性。
综合所有研究，包括我们的研究，miR - 233似乎在血小板功能和HTPR的发展中起适度作用。
