About the journal   Subscriptions   Authors   Users   Librarians   Readers   FAQs 

Clinical Science (2010) 119, (87–95) (Printed in Great Britain)
A translational study of circulating cell-free microRNA-1 in acute myocardial infarction
Yunhui Cheng*1, Ning Tan*†1, Jian Yang*, Xiaojun Liu*, Xiaopei Cao, Pengcheng He, Xiaoli Dong, Shanshan Qin and Chunxiang Zhang
*RNA and Cardiovascular Research Laboratory, Department of Anesthesiology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07101, U.S.A., †Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academic of Medical Sciences, Guangzhou 510100, China, ‡Department of Endocrinology, First Affiliated Hospital, Sun yat-sen University, Guangzhou, 510080, China, and §Sino-American Institute for Translational Medicine, The Affiliated Hospital of Luzhou Medical College, Luzhou 646000, China

Key words: acute myocardial infarction, biomarker, ischaemic preconditioning, ischaemia/reperfusion injury, microRNA, serum.

Abbreviations: AMI, acute myocardial infarction; CK-MB, creatine kinase-MB; i.p., intraperitoneally; I/R, ischaemia/reperfusion; IAR, ischaemic area at risk; IP, ischaemic preconditioning; LAD, left anterior descending coronary artery; miRNA, microRNA; qRT–PCR, quantitative real-time PCR; snoRNA, small nucleolar RNA; TnI, troponin I; TnT, troponin T; TTC, triphenyltetrazolium chloride; VSMC, vascular smooth muscle cell.

1These authors contributed equally to this work.

Correspondence: Dr Chunxiang Zhang (zhangc3@umdnj.edu).


miRNAs (microRNAs) participate in many diseases including cardiovascular disease. In contrast with our original hypothesis, miRNAs exist in circulating blood and are relatively stable due to binding with other materials. The aim of the present translational study is to establish a method of determining the absolute amount of an miRNA in blood and to determine the potential applications of circulating cell-free miR-1 (microRNA-1) in AMI (acute myocardial infarction). The results revealed that miR-1 is the most abundant miRNA in the heart and is also a heart- and muscle-specific miRNA. In a cardiac cell necrosis model induced by Triton X-100 in vitro, we found that cardiac miR-1 can be released into the culture medium and is stable at least for 24 h. In a rat model of AMI induced by coronary ligation, we found that serum miR-1 is quickly increased after AMI with a peak at 6 h, in which an increase in miR-1 of over 200-fold was demonstrated. The miR-1 level returned to basal levels at 3 days after AMI. Moreover, the serum miR-1 level in rats with AMI had a strong positive correlation with myocardial infarct size. To verify further the relationship between myocardial size and miR-1 level, an IP (ischaemic preconditioning) model was used. The results showed that IP significantly reduced circulating miR-1 levels and myocardial infract size induced by I/R (ischaemia/reperfusion) injury. Finally, the levels of circulating cell-free miR-1 were significantly increased in patients with AMI and had a positive correlation with serum CK-MB (creatine kinase-MB) levels. In conclusion, the results suggest that serum miR-1 could be a novel sensitive diagnostic biomarker for AMI.


Received 9 December 2009/9 March 2010; accepted 10 March 2010

Published as Immediate Publication 10 March 2010, doi:10.1042/CS20090645


© The Authors Journal compilation © 2010 Biochemical Society



Chinese users - get faster access here


 RSS feeds

 Table of Contents by email




Latest issues
Vol. 119 No. 12
Vol. 119 No. 11
Vol. 119 No. 10


Immediate Publications
Browse archive
Search archive
Commentaries
Reviews & Hypotheses






Bookmark with:
Bookmark with Del.icio.us Bookmark with Connotea

Opt2Pay


Make it personal - with My Clinical Science!