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

Author

Listed:
  • 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
    Harbin Medical University)

  • Baofeng Yang

    (Harbin Medical University
    Chinese Academy of Medical Sciences, 2019RU070)

  • Yanjie Lu

    (Harbin Medical University)

  • Zhenwei Pan

    (Harbin Medical University
    Chinese Academy of Medical Sciences, 2019RU070)

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.

Suggested Citation

  • 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 , 2021. "The long noncoding RNA lncCIRBIL disrupts the nuclear translocation of Bclaf1 alleviating cardiac ischemia–reperfusion injury," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-020-20844-3
    DOI: 10.1038/s41467-020-20844-3
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    Cited by:

    1. Yamei Liu & Shuya Wang & Jiaxiong Zhang & Quan Sun & Yi Xiao & Jing Chen & Meilian Yao & Guogang Zhang & Qun Huang & Tianjiao Zhao & Qiong Huang & Xiaojing Shi & Can Feng & Kelong Ai & Yongping Bai, 2024. "Reprogramming the myocardial infarction microenvironment with melanin-based composite nanomedicines in mice," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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