Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a. Issue 2 (9th November 2018)

• Record Type: Journal Article
• Authors: Deng, Yao; Luan, Sen; Zhang, Qi; Xiao, Ying
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 2(2019)
• Page Start: 1444
• Page End: 1456
• Publication Date: 2018-11-09
• Subjects: lncRNA THRIL -- lipopolysaccharide -- monocyte chemoattractant protein‐1 -- miR‐34a -- systemic lupus erythematosus; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27354
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with unknown etiology. Nowadays, several long noncoding RNAs (lncRNAs) have been reported as molecular alterations involved in SLE. This study aimed to reveal the function of TNF‐related and HNRNPL‐related immunoregulatory lncRNA (THRIL) in SLE. Human epithelial HK‐2 cells were exposed to lipopolysaccharide (LPS) to mimic an in vitro SLE model. Then, the functions of THRIL, miR‐34a, and monocyte chemoattractant protein‐1 (MCP‐1), as well as their correlations were detected. LncRNA THRIL was highly expressed in the LPS‐stimulated cells, and THRIL overexpression aggravated LPS‐induced cell damage as cell viability was decreased, and apoptosis and the release of proinflammatory cytokines were increased. THRIL worked as a sponge of microRNA‐34a (miR‐34a) and it could directly target MCP‐1. Furthermore, MCP‐1–activated JNK and Wnt/β‐catenin signaling pathways. In conclusion, this study suggested that lncRNA THRIL might be a key regulator participating in LPS‐induced injury in HK‐2 cells. THRIL overexpression aggravated LPS‐induced injury possibly via sponging miR‐34a, and thus preventing MCP‐1 from degradation by miR‐34a. The THRIL/miR‐34a/MCP‐1 axis might play critical roles in SLE. Abstract : The functions of THRIL, miR‐34a, and MCP‐1, as well as their correlations were detected. This study revealed that THRIL aggravated lipopolysaccharide‐induced injury in HK‐2 cells possibly via sponging miR‐34a, thereby leaving and thereby preventing MCP‐1 from degradation by miR‐43a. This finding provides a better understanding of SLE, which will helpful for the treatment of SLE.