• Jie Shen, Jun Yan, Qiuyun Wang, Lei Zhuang, and Yan Luo.
• Department of Anesthesiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
• Shock. 2022 Apr 1; 57 (4): 536543536-543.

AbstractAcute lung injury (ALI) is characterized by excessive production of inflammatory factors and alveolar epithelial damage, type II alveolar epithelial (ATII) cells participate in the repairment of the damaged lung tissue in ALI. Recently, microRNAs (miRNAs) have been found to play crucial roles in the amelioration of various inflammation-induced diseases, including ALI. However, the biological function and the mechanisms of action of miRNAs in the regulation of inflammation, and how ATII cells repair damaged lung tissue in ALI remain unknown. In this study, a model of ALI was established using LPS, and ATII cells were isolated and treated with LPS. Hematoxylin and eosin staining revealed the injury to lung tissues. In this study we found that miR-541-5p expression was significantly decreased in ALI tissue and in the LPS-induced ATII cell model. Additionally, the LPS-induced model showed suppression of ATII cell proliferation and activity. Furthermore, overexpression of miR-541-5p was found to promote cell activity and proliferation in the LPS-induced ATII cell model. Moreover, a luciferase assay illustrated that HMGB1 is a target of miR-541-5p, HMGB1 knockdown blocked the inhibitory effect of miR-541-5p on LPS-induced ATII cells. Ultimately, our study demonstrated that expression of p38, JNK, and ERK in LPS-induced ATII cells increased significantly. These results suggest that miR-541-5p is a key effector in ALI tissue, and that LPS-induced ATII cells act by regulating HMGB1 expression. This effect may be related to excessive activation of the JNK/ERK/p38 signaling pathway.Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Shock Society.

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