Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a
Authors: Ying Xiao
Qi Zhang
Sen Luan
Yao Deng
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: lipopolysaccharide; lncRNA THRIL; miR-34a; monocyte chemoattractant protein-1; systemic lupus erythematosus.
Affiliations: Department of Rheumatology and ImmunologyShengli Oilfield Central HospitalDongying China, Department of NephrologyShengli Oilfield Central HospitalDongying China

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. 

Retracted: Yes

PubPeer comments:
 ![file] Plagiarising [a comment by Elisabeth Bik] : This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: - https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) - https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: - Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 - Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 ,