Research Paper Volume 13, Issue 19 pp 23233—23244
Long non-coding RNA CRNDE as potential biomarkers facilitate inflammation and apoptosis in alcoholic liver disease
- 1 Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
- 2 Department of Forensic Medicine, Wannan Medical College, Wuhu 241002, China
Received: June 26, 2021 Accepted: September 27, 2021 Published: October 11, 2021https://doi.org/10.18632/aging.203614
How to Cite
Copyright: © 2021 Yan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Due to persistent inconsistencies in the expression data of alcoholic liver disease (ALD), it is necessary to turn to “pre-laboratory” comprehensive analysis in order to accelerate effective precision medicine and transformation research. We screened pseudogene-derived lncRNA associated with ALD by comparative analysis of 2 independent data sets from GEO. Three lncRNAs (CRNDE, RBMS3-AS3, and LINC01088) were demonstrated to be potentially useful diagnostic markers in ALD. Among them, the expression of CRNDE is up-regulated. Therefore, we focus on CRNDE. Kyoto Encyclopedia of Genes and Genomes pathways analysis revealed higher CRNDE can activate MAPK signaling pathway, apoptosis, wnt signaling pathway, and hematopoietic cell lineage. Next, we established ALD animal model and verified the success of the modeling. The result showed ALD tissues in mice had significantly higher CRNDE levels than normal tissues. Moreover, the increase of IL-6 in the serum of mice in the low-dose group is related to the activation of inflammatory factors after alcohol-induced liver injury. In addition, alcohol can induce apoptosis, and knockdown of CRNDE can reduce apoptosis. Our integrated expression profiling identified CRNDE independently associated with ALD. CRNDE can facilitate inflammation and apoptosis in ALD.