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Retracted: Knockdown of circular RNA circZNF652 remits LPS‐induced inflammatory damage by regulating miR‐181a
Author(s) -
Liu Xiuxia,
Zhao Peifeng,
Ge Wang
Publication year - 2019
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1606
Subject(s) - gene knockdown , apoptosis , viability assay , lipopolysaccharide , transfection , western blot , flow cytometry , p38 mitogen activated protein kinases , chemistry , inflammation , nf κb , microbiology and biotechnology , immunology , biology , signal transduction , biochemistry , mapk/erk pathway , gene
Background Infantile pneumonia (IP) is a usual disease in infants and young children. The function and underlying mechanism of circZNF652 on lipopolysaccharide (LPS)‐triggered inflammatory damage in WI‐38 cells were detected in this article. Methods WI‐38 cells were induced by dosages of LPS to construct inflammatory injury model. WI‐38 cell viability and apoptosis were detected by CCK‐8 assay and flow cytometry, respectively. CircZNF652 and miR‐181a levels were changed and detected by cell transfection and qRT‐PCR. The levels of apoptosis and JNK/p38 and NF‐κB pathways‐related proteins, as well as the level of Cox‐2 were detected by western blot. Finally, the concentrations of inflammatory factors were detected by ELISA. Results LPS induced inflammatory injury showing as notably decreased the viability, while increased the numbers of apoptotic cells, as well as the levels of apoptosis and inflammatory factors in a dose dependent way. Besides, LPS inducement remarkably enhanced the expression of circZNF652. However, knockdown of circZNF652 remitted LPS‐triggered inflammatory damage and restrained NF‐κB and JNK/p38 pathways. Moreover, circZNF652 knockdown promoted miR‐181a expression. Whereas, miR‐181a inhibition markedly relieved circZNF652 knockdown‐induced impacts. Conclusion Knockdown of circZNF652 remitted LPS‐triggered WI‐38 cells inflammatory damage through deactivation of NF‐κB and JNK/p38pathways by up‐regulating miR‐181a.