The Emerging Role of miR-223 in Platelet Reactivity: Implications in Antiplatelet Therapy

• Published in: BioMed research international Vol. 2015; no. 2015; pp. 1 - 8
• Main Authors: Li, Yu-Ming, Ma, Yong-Qiang, Zhang, Ying-Ying, Ji, Wen-Jie, Zhou, Xin, Shi, Rui, Zhang, Jian-Qi
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2015; Hindawi Limited
• Subjects: Biosynthesis; Blood Platelets - metabolism; Blood Platelets - pathology; Bone marrow; Cardiovascular disease; Coronary Disease - drug therapy; Coronary Disease - genetics; Coronary Disease - pathology; Gene expression; Gene Expression Regulation - genetics; Humans; Inflammatory diseases; Insulin-like growth factors; Kinases; Laboratories; Megakaryocytes - metabolism; MicroRNAs - genetics; Platelet Aggregation Inhibitors - therapeutic use; Proteins; Receptors, Purinergic P2Y12 - drug effects; Receptors, Purinergic P2Y12 - genetics; Review; Stem cells; Studies
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2015/981841

Platelets are anuclear cells and are devoid of genomic DNA, but they are capable of de novo protein synthesis from mRNA derived from their progenitor cells, megakaryocytes. There is mounting evidence that microRNA (miRNA) plays an important role in regulating gene expression in platelets. miR-223 is the most abundant miRNAs in megakaryocytes and platelets. One of the miR-223-regulated genes is ADP P2Y12, a key target for current antiplatelet drug therapy. Recent studies showed that a blunted response to P2Y12 antagonist, that is, high on-treatment platelet reactivity (HTPR), is a strong predictor of major cardiovascular events (MACEs) in coronary heart disease (CHD) patients receiving antiplatelet treatment. Recent clinical cohort study showed that the level of circulating miR-223 is inversely associated with MACE in CHD patients. In addition, our recent data demonstrated that the level of both intraplatelet and circulating miR-223 is an independent predictor for HTPR, thus providing a link between miR-223 and MACE. These lines of evidence indicate that miR-223 may serve as a potential regulatory target for HTPR, as well as a diagnostic tool for identification of HTPR in clinical settings.