Long noncoding RNA TUG1 is downregulated in sepsis and may sponge miR-27a to downregulate tumor necrosis factor-α. Issue 4 (April 2020)

• Record Type: Journal Article
• Authors: Wang, Li; Zhong, Qinghua; Feng, Yanli; Tang, Xiaoying; Wang, Qiong; Zou, Yongyi; Duan, Jiang
• Is Part Of: Journal of international medical research. Volume 48:Issue 4(2020)
• Publication Date: 2020-04
• Subjects: Sepsis -- survival -- taurine-upregulated gene 1 (TUG1) -- miR-27a -- tumor necrosis factor-α (TNF-α) -- long noncoding RNA; Medicine -- Periodicals; Pharmacology -- Periodicals; 610.5
• DOI: 10.1177/0300060520910638
• Languages: English
• ISSNs: 0300-0605

Abstract

Objectives: Bioinformatics analysis revealed a potential interaction between long noncoding (lnc)RNA TUG1 (taurine-upregulated gene 1) and microRNA (miR)-27a. miR-27a can promote sepsis by upregulating tumor necrosis factor-α (TNF-α). Our objective was to study the roles of TUG1 in sepsis. Methods: Plasma levels of TUG1 in patients with sepsis and in healthy controls were measured by quantitative PCR assay. The IntaRNA program was used to predict potential interactions between TUG1 mRNA and miR-27a. The interaction between TUG1 and miR-27a was further explored by transfecting TUG1 expression vector or miR-27a mimic into AC16 human cardiomyocytes, and apoptosis was evaluated by cell apoptosis assay. Results: TUG1 was downregulated in patients with sepsis. TUG1 was able to directly interact with miR-27a, but overexpression of TUG1 or miR-27a failed to affect the expression of each other. In contrast, TUG1 overexpression led to decreased levels of TNF-α, whereas miR-27a overexpression increased TNF-α in cardiomyocytes. Cell apoptosis analysis showed that TNF-α and miR-27a overexpression promoted apoptosis of cardiomyocytes induced by lipopolysaccharide. TUG1 overexpression had the opposite effect and attenuated the effects of TNF-α and miR-27a overexpression. Conclusion: We conclude that TUG1 is downregulated in sepsis and may act as a molecular "sponge" of miR-27a to downregulate TNF-α.