The upregulation of miR-204-3p in LPS-induced acute lung injury aggravated pulmonary endothelial cells apoptosis via targeting sulfatase 2

Liya  Zhang; Zhengyu  Zhu; Qian Zhang; Zhengdao  Mao

doi:10.18388/abp.2020_5518

Liya Zhang Department of Emergency Medicine, Nanjing Medical University Affiliated Changzhou No. 2 People’s Hospital, Changzhou, Jiangsu Province, 213164, China
Zhengyu Zhu Department of Pediatrics, Nanjing Medical University Affiliated Changzhou No. 2 People’s Hospital, Changzhou, Jiangsu Province, 213164, China
Qian Zhang Department of Respiratory Medicine, Nanjing Medical University Affiliated Changzhou No. 2 People’s Hospital, Changzhou, Jiangsu Province, 213164, China https://orcid.org/0000-0002-1771-2130
Zhengdao Mao Department of Respiratory Medicine, Nanjing Medical University Affiliated Changzhou No. 2 People’s Hospital, Changzhou, Jiangsu Province, 213164, China

DOI: https://doi.org/10.18388/abp.2020_5518

Abstract

Acute lung injury (ALI) results from the injury of alveolar epithelial cells and pulmonary capillary endothelial cells, with a high mortality rate ranging from 29% to 42%. Therefore, more efficient therapeutic strategies for ALI are necessary. Numerous studies revealed that miRNAs play a role in the regulation of ALI. Lipopolysaccharide (LPS) can induce an inflammatory response and has been widely applied in the establishment of the mouse ALI model. Here, we reported that miR-204-3p expression was upregulated by LPS treatment with increased cytokine secretion. LPS treatment promoted cell apoptosis, accompanied by abnormal cell structure and unobvious alveolar structure. These effects could be prevented by down-regulation of miR-204-3p, and promoted by miR-204-3p overexpression. Sulfatase 2 (SULF2) appeared to be the target of miR-204-3p predicted by TargetScan. Downregulation of miR-204-3p enhanced the protein level of SULF2, indicating that SULF2 was a target of miR-204-3p, which could negatively regulate the expression of SULF2. Thus, targeting miR-204-3p may be a potential therapeutic strategy for ALI.