LncRNA THRIL is upregulated in sepsis and sponges miR-19a to upregulate TNF-α in human bronchial epithelial cells

• Published in: Journal of inflammation (London, England) Vol. 17; no. 1; pp. 31 - 7
• Main Authors: Liu, Tao, Liu, Jingbin, Tian, Chunhua, Wang, Hongyuan, Wen, Min, Yan, Mingyu
• Format: Journal Article
• Language: English
• Published: London BioMed Central 10.09.2020; BMC
• Subjects: Allergology; Apoptosis; Bioinformatics; Biomedical and Life Sciences; Biomedicine; Cytokines and Growth Factors; Disease; Epithelial cells; Gastroenterology; Immunology; Immunoregulation; Inflammation; Lipopolysaccharides; lncRNA THRIL; MicroRNAs; miR-19a; Mortality; Non-coding RNA; Pharmacology/Toxicology; Physiology; Plasma; Proteins; Rheumatology; Sepsis; TNF-α; Tumor necrosis factor-α; United States > US; Sepsis; lncRNA THRIL; TNF-α; miR-19a; Apoptosis
• ISSN: 1476-9255; 1476-9255
• DOI: 10.1186/s12950-020-00259-z

Background Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in various diseases. Our bioinformatics analysis showed that lncRNA TNFα and heterogenous nuclear ribonucleoprotein L (hnRNPL) related immunoregulatory LincRNA (THRIL) may interact with miR-19a, which targets TNF-α. This study aimed to explore the role of THRIL, an enhancer of LPS-induced inflammatory, in sepsis. Methods Research subjects of the present study included 66 sepsis patients and 66 healthy volunteers. The expression levels of THRIL, miR-19a and TNF-α in plasma samples from these participants were determined by RT-qPCR. The interaction between THRIL and miR-19a was explored by performing overexpression experiments in human bronchial epithelial cells (HBEpCs). The roles of THRIL, miR-19a and TNF-α in regulating the apoptosis of HBEpCs were analyzed by cell apoptosis assay. Results We found that THRIL was upregulated in sepsis patients. THRIL is predicted to interact with miR-19a, and the interaction was confirmed by dual-luciferase activity assay. However, THRIL and miR-19a did not affect the expression of each other. Instead, overexpression of THRIL resulted in the increased expression levels of TNF-α, a downstream target of miR-19a in HBEpCs. In HBEpCs, LPS treatment induced the overexpression of THRIL. Cell apoptosis analysis showed that overexpression of THRIL and TNF-α promoted the apoptosis of HBEpCs induced by LPS, while overexpression of miR-19a played an opposite role. Overexpression of THRIL attenuated the effects of overexpression of miR-19a. Conclusion Therefore, THRIL is upregulated in sepsis and may sponge miR-19a to upregulate TNF-α, thereby promoting lung cell apoptosis.