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RETRACTED ARTICLE: Long non-coding RNA NKILA weakens TNF-α-induced inflammation of MRC-5 cells by miR-21 up-regulation

Dandan Wang, Jiajie Zhang, Yan Sun, Nan Lv, Jianwei Sun

2020Artificial Cells Nanomedicine and Biotechnology15 citationsDOIOpen Access PDF

Abstract

Background Infantile pneumonia (IP) seriously affects the health of children. This article mainly discussed the protective effect of long non-coding RNA NKILA (lnc NKILA) on IP by detecting cell viability, apoptosis and inflammatory response of MRC5 cells.Methods Cell counting kit-8 (CCK-8) was used to detect cell viability, while flow cytometry was used to detect cell apoptosis. The expression of apoptosis-associated factors (Bcl-2, Bax, PARP and Cleaved-PARP) and NF-κB and JNK pathway-related factors (t-IκBα, p-IκBα, t-p65, p-p65, β-actin, t-JNK and p-JNK) were tested by western blot. Otherwise, productions of inflammatory factors interleukin (IL)-1β and IL-6 were tested by enzyme-linked immunosorbent assay (ELISA) and western blot. Furthermore, RNA levels were respectively tested and changed by RT-qPCR and cell transfection.Results Tumour necrosis factor-α (TNF-α) treatment reduced cell viability, induced cell apoptosis and promoted inflammatory factors expression. NKILA overexpression remitted TNF-α-induced injury. Moreover, NKILA positively regulated miR-21. miR-21 inhibition could weaken the functions of NKILA overexpression on TNF-α-induced injury. At last, NKILA and miR-21 were involved in the regulation of JNK and NF-κB pathways.Conclusions NKILA overexpression remitted TNF-α-induced MRC5 cell injury by up-regulation of miR-21 and via inactivation of JNK and NF-κB signaling pathways.

Topics & Concepts

Viability assayApoptosisTumor necrosis factor alphaFlow cytometryWestern blotCellCell biologyChemistryTransfectionBiologyCancer researchMolecular biologyImmunologyCell cultureGeneBiochemistryGeneticsCancer-related molecular mechanisms researchImmune Response and InflammationMicroRNA in disease regulation