Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide-induced HK-2 cells injury by sponging miR-34a |
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Authors: | Yao Deng Sen Luan Qi Zhang Ying Xiao |
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Affiliation: | 1. Department of Rheumatology and Immunology, Shengli Oilfield Central Hospital, Dongying, China;2. Department of Nephrology, Shengli Oilfield Central Hospital, Dongying, China |
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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. |
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Keywords: | lncRNA THRIL lipopolysaccharide monocyte chemoattractant protein-1 miR-34a systemic lupus erythematosus |
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