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Research Paper

Silencing of LncRNA FGD5-AS1 prevents inflammation in acute pneumonia via targeting miR-301a-3p/TNFα

Qing-Min Liu1, Yi-Yu He2, Li-Li Liu3, Li-Kun Wang3
  • 1Intensive Care Unit, Linyi People's Hospital, Linyi, Shandong Province, China
  • 2Department of Cardiovescular Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China
  • 3Department of Pathology, Linyi People's Hospital, Linyi, Shandong Province, China
  • 4Department of Infection Control Center, Linyi People's Hospital, Linyi, Shandong Province, China
* Equal contribution
Received: May 15, 2020Accepted: July 21, 2020
https://doi.org/10.18632/aging.202310

Copyright: © 2021 Liu 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.

Abstract

Long non-coding RNA (LncRNA) regulates the expression of specific genes in the process of transcriptional recruitment, expression, post-transcriptional modification and epigenetics, and is widely involved in various physiological and pathological processes. The morbidity and mortality of acute pneumonia caused by sepsis are high. At present, the pathogenesis of severe pneumonia is not clear, and there is a lack of specific treatment. In this research, we observed that The expression of lncRNA FGD5-AS1 was significantly increased in LPS-mouse models. Forced decreased of FGD5-AS1 alleviated the lung function and lung injury, reduced inflammatory cell infiltration, and production of TNFα. Next, mice were exposed with TNFα neutralizing antibody after LPS treatment. TNFα neutralizing antibody prevents lung injury and inflammation induced by LPS.

Further, we found miR-301a-3p was down-regulated in LPS mice, which could interact with FGD5-AS1. Meanwhile, the results of the analysis of multiple target prediction websites show that TNFα was an underlying target of miR-301a-3p. In conclusion, FGD5-AS1 regulated TNF-α and remitted inflammation in pneumonia by monitoring miR-301a-3p.