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长链非编码 RNA lncCIRBIL 破坏 Bclaf1 的核转位，从而减轻心脏缺血再灌注损伤。

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

机构信息

Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, Harbin, 150086, China.

Institute of Metabolic Disease, Heilongjiang Academy of Medical Science, Harbin Medical University Cancer Hospital, Harbin, China.

出版信息

Nat Commun. 2021 Jan 22;12(1):522. doi: 10.1038/s41467-020-20844-3.

DOI:10.1038/s41467-020-20844-3
PMID:33483496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7822959/
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.

摘要

心肌缺血再灌注（I/R）损伤是导致心肌细胞死亡的病理过程。本研究旨在评估长链非编码 RNA 心脏损伤相关 Bclaf1 抑制长非编码 RNA（lncCIRBIL）在心肌 I/R 损伤中的作用，并阐明其作用机制。lncCIRBIL 在 I/R 心脏中的水平降低。心肌细胞特异性过表达 lncCIRBIL 可减少 I/R 损伤后的梗死面积。lncCIRBIL 在小鼠中的敲除会加重心肌 I/R 损伤。在体外也观察到了相同的定性结果。lncCIRBIL 直接与 BCL2 相关转录因子 1（Bclaf1）结合，抑制其核易位。心肌细胞特异性过表达 Bclaf1 会加重，而 Bclaf1 的部分敲除则减轻心肌 I/R 损伤。同时，Bclaf1 的部分敲除消除了 lncCIRBIL 敲除对心肌 I/R 损伤的不良影响。总之，lncCIRBIL 通过抑制 Bclaf1 的核易位对 I/R 损伤发挥保护作用。lncCIRBIL 和 Bclaf1 是缺血性心脏病的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/4d738bca7b69/41467_2020_20844_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/807a6fb50774/41467_2020_20844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/4dca76e73d56/41467_2020_20844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/968814e0e5ca/41467_2020_20844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/825a065c3b71/41467_2020_20844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/19257088602e/41467_2020_20844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/ed3e2b7eb2f2/41467_2020_20844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/5476d6a42b87/41467_2020_20844_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/4d738bca7b69/41467_2020_20844_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/807a6fb50774/41467_2020_20844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/4dca76e73d56/41467_2020_20844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/968814e0e5ca/41467_2020_20844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/825a065c3b71/41467_2020_20844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/19257088602e/41467_2020_20844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/ed3e2b7eb2f2/41467_2020_20844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/5476d6a42b87/41467_2020_20844_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df25/7822959/4d738bca7b69/41467_2020_20844_Fig8_HTML.jpg

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