Long non-coding RNA CCRR controls cardiac conduction via regulating intercellular coupling

Yong Zhang, Lihua Sun, Lina Xuan, Zhenwei Pan, Xueling Hu, Hongyu Liu, Yunlong Bai, Lei Jiao, Zhange Li, Lina Cui, Xiaoxue Wang, Siqi Wang, Tingting Yu, Bingbing Feng, Ying Guo, Zonghong Liu, Weixin Meng, Hequn Ren, Jiyuan Zhu, Xuyun Zhao, Chao Yang, Ying Zhang, Chaoqian Xu, Zhiguo Wang, Yanjie Lu, Hongli Shan () and Baofeng Yang ()
Additional contact information
Yong Zhang: Harbin Medical University
Lihua Sun: Harbin Medical University
Lina Xuan: Harbin Medical University
Zhenwei Pan: Harbin Medical University
Xueling Hu: Harbin Medical University
Hongyu Liu: Harbin Medical University
Yunlong Bai: Harbin Medical University
Lei Jiao: Harbin Medical University
Zhange Li: Harbin Medical University
Lina Cui: Harbin Medical University
Xiaoxue Wang: Harbin Medical University
Siqi Wang: Harbin Medical University
Tingting Yu: Harbin Medical University
Bingbing Feng: Harbin Medical University
Ying Guo: Harbin Medical University
Zonghong Liu: Harbin Medical University
Weixin Meng: Harbin Medical University
Hequn Ren: Harbin Medical University
Jiyuan Zhu: Harbin Medical University
Xuyun Zhao: Harbin Medical University
Chao Yang: Harbin Medical University
Ying Zhang: Harbin Medical University
Chaoqian Xu: Mu Danjiang Medical University Mu Danjiang
Zhiguo Wang: Harbin Medical University
Yanjie Lu: Harbin Medical University
Hongli Shan: Harbin Medical University
Baofeng Yang: Harbin Medical University

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Long non-coding RNAs (lncRNAs) have emerged as a new class of gene expression regulators playing key roles in many biological and pathophysiological processes. Here, we identify cardiac conduction regulatory RNA (CCRR) as an antiarrhythmic lncRNA. CCRR is downregulated in a mouse model of heart failure (HF) and in patients with HF, and this downregulation slows cardiac conduction and enhances arrhythmogenicity. Moreover, CCRR silencing induces arrhythmias in healthy mice. CCRR overexpression eliminates these detrimental alterations. HF or CCRR knockdown causes destruction of intercalated discs and gap junctions to slow longitudinal cardiac conduction. CCRR overexpression improves cardiac conduction by blocking endocytic trafficking of connexin43 (Cx43) to prevent its degradation via binding to Cx43-interacting protein CIP85, whereas CCRR silence does the opposite. We identified the functional domain of CCRR, which can reproduce the functional roles and pertinent molecular events of full-length CCRR. Our study suggests CCRR replacement a potential therapeutic approach for pathological arrhythmias.

Date: 2018
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DOI: 10.1038/s41467-018-06637-9

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