LncRNA H19 aggravates TNF ‐α‐induced inflammatory injury via TAK1 pathway in MH7A cells

AbstractRheumatoid arthritis (RA) is a common chronic autoimmune disease in women. This research aims to disclose the probable function of lncRNA H19 in MH7A cells.The influences of tumor necrosis factor ‐α (TNF‐α) on cell viability, apoptosis, and inflammatory factor expression were, respectively, detected through cell counting kit‐8 (CCK‐8), flow cytometry, quantitative reverse transcription polymerase chain reaction (qRT‐PCR), enzyme‐linked immunosorbent assay (ELISA) assay and West ern Blot. The levels of H19 and TAK1 were, respectively, tested through qRT‐PCR and Western blot. The expression of NF‐κB and JNK/p38MAPK pathway‐associated proteins was tested through Western blot. We found that TNF‐α reduced MH7A cell viability in a concentration‐dependent manner and f acilitated apoptosis and IL‐8, IL‐1β, and IL‐6 production. Besides, TNF‐α treatment raised the level of H19 in MH7A cells. Moreover, H19 silence reduced the levels of inflammatory cytokines, while overexpression of H19 reversed this effect. TNF‐α treatment elevated the expression of inf lammatory cytokines by up‐regulating H19. Furthermore, overexpression of H19 promoted TAK1 phosphorylation. Following studies revealed that H19 activated NF‐κB and JNK/p38 MAPK pathways by promoting TAK1 phosphorylation.

Source: BioFactors - June 10, 2020 Category: Biochemistry Authors: Jialiang Yang, Yixuan Li, Lili Wang, Zhenchun Zhang, Zunzhong Li, Qian Jia Tags: Research Communication Source Type: research