Abstract
// Zhi-Xiao Li 1, * , Qiong Lin 2, * , Zhi-Gang He 1 , Quan Wang 1 , Ying-Le Chen 3 , Mao-Hui Feng 4 , Shun-Yuan Li 3 and Hong-Bing Xiang 1 1 Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 2 Department of Anesthesiology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China 3 Department of Anesthesiology, The First Affiliated Quanzhou Hospital of Fujian Medical University, Quanzhou 362000, China 4 Department of Oncology, Wuhan Peritoneal Cancer Clinical Medical Research Center, Zhongnan Hospital of Wuhan University, Hubei Key Laboratory of Tumor Biological Behaviors and Hubei Cancer Clinical Study Center, Wuhan 430071, China * These authors contributed equally to this work Correspondence to: Shun-Yuan Li, email: cylfj@126.com Hong-Bing Xiang, email: xhbtj2004@163.com Keywords: cardiac ischemia/reperfusion injury; differentially expressed genes; lncRNAs; real-time quantitative PCR Received: October 07, 2017 Accepted: November 13, 2017 Published: January 03, 2018 ABSTRACT We used Agilent Gene Expression microarray to analyze differential gene and lncRNA expression patterns in the myocardial ischemia regions during ischemia/reperfusion (I/R)-induced cardiac injury in rats. Male SD rats were assigned into control group, 2 h group (30 min ischemia followed by 2 h reperfusion), 0.5 h (30 min ischemia followed by 0.5h reperfusion) group. We observed that of 18090 lncRNAs, an average of 233 lncRNAs was up-regulated in ischemic tissues of 2 h group, compared with those in control group, while an average of 6115 lncRNAs was down-regulated (with a > 2.0 fold-change and p < 0.05). Further, a total of 3135 mRNAs were differentially expressed between control group and 2h group, in which 542 mRNAs were up-regulated and 2593 mRNAs were down-regulated. Some differentially expressed genes were validated by qRT-PCR analyses of select lncRNAs in different time points after cardiac I/R injury. We unveiled that the expressions of lncRNA XR_345533.2, NONRATT025386, NONRATT024318, XR_599241.1, and NONRATT025509 were significantly up-regulated in 2h group compared with control group and 0.5h group, whereas the expression of lncRNA NR_130708.1 was down-regulated after cardiac I/R injury and had no statistically different between 0.5h group and 2h group. Otherwise, the expressions of lncRNA NONRATT028627, NONRATT021959, XR_590005.1 and NONRATT023191 were significantly up-regulated in 2h group compared with 0.5h group. These findings provide evidence for differential expression patterns of mRNAs and lncRNAs in the ischemic tissues after cardiac I/R injury in rats.
Highlights
Cardiomyocyte death due to ischemia/reperfusion (I/R) injury is well-known to increase morbidity, mortality and medical cost in patients with ischemic heart disease [1,2,3,4]
We unveiled that the expressions of long non-coding RNAs (lncRNAs) XR_345533.2, NONRATT025386, NONRATT024318, XR_599241.1, and NONRATT025509 were significantly up-regulated in 2h group compared with control group and 0.5h group, whereas the expression of lncRNA NR_130708.1 was downregulated after cardiac ischemia/ reperfusion (I/R) injury and had no statistically different between 0.5h group and 2h group
In order to select out possible targets of lncRNAs between model and control group, up to 18090 coding transcripts were detected in the ischemic tissues of the heart at 2h after reperfusion
Summary
Cardiomyocyte death due to ischemia/reperfusion (I/R) injury is well-known to increase morbidity, mortality and medical cost in patients with ischemic heart disease [1,2,3,4]. Treatment for this myocardial ischemia-reperfusion disorder and cardiomyocyte death has had limited success. The pathological process leading to cardiomyocyte death is very complicated and our understanding of the mechanisms that underlie the induction of cardiomyocyte death is incomplete [5, 6]. The molecular mechanisms that underlie this regulation for myocardial ischemia-reperfusion disorder are still unknown
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