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

Abstract

Rheumatoid 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 Western 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 facilitated 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 inflammatory 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.