Premium
Retracted : Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a
Author(s) -
Deng Yao,
Luan Sen,
Zhang Qi,
Xiao Ying
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27354
Subject(s) - proinflammatory cytokine , lipopolysaccharide , microrna , long non coding rna , apoptosis , wnt signaling pathway , microbiology and biotechnology , monocyte , immunology , inflammation , regulator , chemistry , cancer research , signal transduction , downregulation and upregulation , biology , gene , biochemistry
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.