The long noncoding RNA lncCIRBIL disrupts the nuclear translocation of Bclaf1 alleviating cardiac ischemia–reperfusion injury

Yang Zhang, Xiaofang Zhang, Benzhi Cai, Ying Li, Yuan Jiang, Xiaoyu Fu, Yue Zhao, Haiyu Gao, Ying Yang, Jiming Yang, Shangxuan Li, Hao Wu, Xuexin Jin, Genlong Xue, Jiqin Yang, Wenbo Ma, Qilong Han, Tao Tian, Yue Li, Baofeng Yang (), Yanjie Lu and Zhenwei Pan ()
Additional contact information
Yang Zhang: Harbin Medical University
Xiaofang Zhang: Harbin Medical University
Benzhi Cai: Harbin Medical University
Ying Li: Harbin Medical University
Yuan Jiang: Harbin Medical University
Xiaoyu Fu: Harbin Medical University
Yue Zhao: Harbin Medical University
Haiyu Gao: Harbin Medical University
Ying Yang: Harbin Medical University
Jiming Yang: Harbin Medical University
Shangxuan Li: Harbin Medical University
Hao Wu: Harbin Medical University
Xuexin Jin: Harbin Medical University
Genlong Xue: Harbin Medical University
Jiqin Yang: Harbin Medical University
Wenbo Ma: Harbin Medical University
Qilong Han: Harbin Medical University
Tao Tian: Harbin Medical University
Yue Li: Harbin Medical University Cancer Hospital
Baofeng Yang: Harbin Medical University
Yanjie Lu: Harbin Medical University
Zhenwei Pan: Harbin Medical University

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Cardiac ischemia–reperfusion (I/R) injury is a pathological process resulting in cardiomyocyte death. The present study aims to evaluate the role of the long noncoding RNA Cardiac Injury-Related Bclaf1-Inhibiting LncRNA (lncCIRBIL) on cardiac I/R injury and delineate its mechanism of action. The level of lncCIRBIL is reduced in I/R hearts. Cardiomyocyte-specific transgenic overexpression of lncCIRBIL reduces infarct area following I/R injury. Knockout of lncCIRBIL in mice exacerbates cardiac I/R injury. Qualitatively, the same results are observed in vitro. LncCIRBIL directly binds to BCL2-associated transcription factor 1 (Bclaf1), to inhibit its nuclear translocation. Cardiomyocyte-specific transgenic overexpression of Bclaf1 worsens, while partial knockout of Bclaf1 mitigates cardiac I/R injury. Meanwhile, partial knockout of Bclaf1 abrogates the detrimental effects of lncCIRBIL knockout on cardiac I/R injury. Collectively, the protective effect of lncCIRBIL on I/R injury is accomplished by inhibiting the nuclear translocation of Bclaf1. LncCIRBIL and Bclaf1 are potential therapeutic targets for ischemic cardiac disease.

Date: 2021
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DOI: 10.1038/s41467-020-20844-3

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