Lin Yang1, Li Zhao1, Hui Zhang1, Peili Chen1. 1. Department of Critical Care Medicine, The First People's Hospital of Shangqiu Shangqiu 476100, Henan Province, China.
Abstract
BACKGROUND: Acute lung injury (ALI) caused by sepsis is the most common disease and the leading cause of death in intensive care units. Recent studies have revealed that long non-coding RNAs (LncRNAs) are abnormally expressed in sepsis. This study aimed to clarify the role and mechanism of Taurine up-regulated gene 1 (TUG1) in ALI caused by sepsis. METHODS: Lipopolysaccharide (LPS) was used to simulate sepsis-induced ALI model. RT-PCR, Dual luciferase reporter (DLR) assay and RNA immunoprecipitation (RIP) were used to detect TUG1 and miR-494. The rat model with sepsis-induced ALI was established by intraperitoneal injection of LPS to verify the results of in vitro experiments. RESULTS: The expressions of TUG1 and PDK4 were down-regulated while the expression of miR-494 was up-regulated in lung tissues and human small airway epithelial cells (HSAECs). TUG1 was indirectly mediated. Overexpression of TUG1 or inhibition of miR-494 could significantly improve the survival rate of HSAECs. Transfection of miR-494 mimics achieved the opposite effect. Enzyme-linked immunosorbent assay (ELISA) showed that the expression of arthritis-related factors in rats was increased after up-regulating TUG1. CONCLUSION: TUG1 is lowly expressed in sepsis. Up-regulating TUG1 can alleviate the inflammatory response in ALI caused by LPS-induced sepsis, which may be a clinical treatment target. AJTR
BACKGROUND: Acute lung injury (ALI) caused by sepsis is the most common disease and the leading cause of death in intensive care units. Recent studies have revealed that long non-coding RNAs (LncRNAs) are abnormally expressed in sepsis. This study aimed to clarify the role and mechanism of Taurine up-regulated gene 1 (TUG1) in ALI caused by sepsis. METHODS: Lipopolysaccharide (LPS) was used to simulate sepsis-induced ALI model. RT-PCR, Dual luciferase reporter (DLR) assay and RNA immunoprecipitation (RIP) were used to detect TUG1 and miR-494. The rat model with sepsis-induced ALI was established by intraperitoneal injection of LPS to verify the results of in vitro experiments. RESULTS: The expressions of TUG1 and PDK4 were down-regulated while the expression of miR-494 was up-regulated in lung tissues and human small airway epithelial cells (HSAECs). TUG1 was indirectly mediated. Overexpression of TUG1 or inhibition of miR-494 could significantly improve the survival rate of HSAECs. Transfection of miR-494 mimics achieved the opposite effect. Enzyme-linked immunosorbent assay (ELISA) showed that the expression of arthritis-related factors in rats was increased after up-regulating TUG1. CONCLUSION: TUG1 is lowly expressed in sepsis. Up-regulating TUG1 can alleviate the inflammatory response in ALI caused by LPS-induced sepsis, which may be a clinical treatment target. AJTR
Authors: Mervyn Singer; Clifford S Deutschman; Christopher Warren Seymour; Manu Shankar-Hari; Djillali Annane; Michael Bauer; Rinaldo Bellomo; Gordon R Bernard; Jean-Daniel Chiche; Craig M Coopersmith; Richard S Hotchkiss; Mitchell M Levy; John C Marshall; Greg S Martin; Steven M Opal; Gordon D Rubenfeld; Tom van der Poll; Jean-Louis Vincent; Derek C Angus Journal: JAMA Date: 2016-02-23 Impact factor: 56.272
Authors: Meng Du; Lin Yuan; Xin Tan; Dandan Huang; Xiaojing Wang; Zhe Zheng; Xiaoxiang Mao; Xiangrao Li; Liu Yang; Kun Huang; Fengxiao Zhang; Yan Wang; Xi Luo; Dan Huang; Kai Huang Journal: Nat Commun Date: 2017-12-11 Impact factor: 14.919