Profiling of differentially expressed microRNAs in arrhythmogenic right ventricular cardiomyopathy.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a kind of primary cardiomyopathy characterized by the fibro-fatty replacement of right ventricular myocardium. Currently, myocardial microRNAs have been reported to play critical role in the pathophysiology of cardiovascular pathophysiology. So far, the profiling of microRNAs in ARVC has not been described. In this study, we applied S-Poly (T) Plus method to investigate the expression profile of microRNAs in 24 ARVC patients heart samples. The tissue levels of 1078 human microRNAs were assessed and were compared with levels in a group of 24 healthy controls. Analysis of the area under the receiver operating characteristic curve (ROC) supported the 21 validated microRNAs to be miRNA signatures of ARVC, eleven microRNAs were significantly increased in ARVC heart tissues and ten microRNAs were significantly decreased. After functional enrichment analysis, miR-21-5p and miR-135b were correlated with Wnt and Hippo pathway, which might involve in the molecular pathophysiology of ARVC. Overall, our data suggested that myocardial microRNAs were involved in the pathophysiology of ARVC, miR-21-5p and miR-135b were significantly associated with both the myocardium adipose and fibrosis, which was a potential disease pathway for ARVC and might to be useful as therapeutic targets for ARVC.
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.|Department of Cardiology, the First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, 154002, People's Republic of China.|Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, 518060, People's Republic of China.
Hongliang
H
Zhang
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Shenghua
S
Liu
Department of Cardiology, the First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, 154002, People's Republic of China.
Tianwei
T
Dong
Department of Cardiology, the First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, 154002, People's Republic of China.
Jun
J
Yang
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Yuanyuan
Y
Xie
Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, 518060, People's Republic of China.
Yike
Y
Wu
Department of Physiology, Shenzhen University Health Science Center, Shenzhen, Guangdong 518060, People's Republic of China.
Kang
K
Kang
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Shengshou
S
Hu
Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, 518060, People's Republic of China.
Deming
D
Gou
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Yingjie
Y
Wei
D050156:Adipogenesis / Q000235:genetics*; D000273:Adipose Tissue / Q000473:pathology; D000328:Adult; D019571:Arrhythmogenic Right Ventricular Dysplasia / Q000235:genetics*; D005260:Female; D005355:Fibrosis / Q000235:genetics* / Q000473:pathology; D000090683:Hippo Signaling Pathway; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D024510:Muscle Development / Q000235:genetics; D009206:Myocardium / Q000473:pathology*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D060449:Wnt Signaling Pathway / Q000235:genetics; D055815:Young Adult
C544965:MIRN135 microRNA, human; C524940:MIRN21 microRNA, human; D035683:MicroRNAs; D017346:Protein Serine-Threonine Kinases