Identification of cardiac long non-coding RNA profile in human dilated cardiomyopathy

Abstract

Aims Dilated cardiomyopathy (DCM) induced chronic heart failure is a life-threatening disease worldwide. Long non-coding RNAs (lncRNAs) are potential new therapeutic targets and may provide new pathophysiological mechanisms for development of DCM. Methods and results Microarray assays in 14 DCM and 10 control human heart samples identified 313 significantly differentially expressed lncRNAs. SiRNAs were used to explore the potential function of specific lncRNAs (RP11-544D21.2 and XLOC-014288) in human cardiac myocytes, human cardiac fibroblasts and human cardiac microvascular endothelial cells, respectively. RNA-seq and pathway analyses revealed the function of lncRNA RP11-544D21.2 and XLOC-014288 in three heart cells. Furthermore, impaired tube formation and migration were observed in si-RP11-544D21.2-treated endothelial cells. Moreover, TAF10 was predicted and verified to be one of the causes of some up-regulated lncRNAs. Then, we found that the left ventricular ejection fraction correlated with these changed lncRNAs. Conclusions This study provides a comparison of human cardiac lncRNA profiles in control and DCM. It illustrates the function and complex roles of the differentially expressed lncRNAs in different cell types in the heart, which may lead to new insights into the mechanisms and treatment strategies for DCM in the future.