LncRNA H19 aggravates TNF‐α‐induced inflammatory injury via TAK1 pathway in MH7A cells. (11th June 2020)

• Record Type: Journal Article
• Authors: Yang, Jialiang; Li, Yixuan; Wang, Lili; Zhang, Zhenchun; Li, Zunzhong; Jia, Qian
• Is Part Of: BioFactors. Volume 46:Number 5(2020)
• Page Start: 813
• Page End: 820
• Publication Date: 2020-06-11
• Subjects: JNK/p38MAPK pathway -- LncRNA H19 -- NF‐κB pathway -- rheumatoid arthritis -- TAK1 -- TNF‐α; Vitamins -- Physiological effect -- Periodicals; Trace elements -- Physiological effect -- Periodicals; Growth factors -- Physiological effect -- Periodicals; Plant growth promoting substances -- Physiological effect -- Periodicals; Biochemistry -- Periodicals; Nutritional Physiological Phenomena -- Periodicals; Trace Elements -- metabolism -- Periodicals; Vitamins -- metabolism -- Periodicals; Molecular Biology -- Periodicals; 612.399
• DOI: 10.1002/biof.1659
• Languages: English
• ISSNs: 0951-6433

Abstract

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.