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ABSTRACT: Introduction
Overexpressed inflammatory cytokines are the main factors causing rheumatoid arthritis (RA) tissue damage and pathological deterioration, and lncRNAs has found to beinvolved in some autoinflammatory diseases.Methods
We designed this study to investigate the effect of lncRNA linc00152 on rheumatoid arthritis inflammation and explore its molecular mechanism.Result
We found that linc00152 was not only up-regulated in rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), but also stimulated by TNF-α/IL-1β in adose- and time-dependent manner in RAFLS and this expression depends on the NF-κB signaling pathway. Conversely, linc00152 promoted TNF-α/IL-1β expression in RAFLS induced by TNF-α/IL-1β. In addition, we found that linc00152 promoted TAK1 expressi
SUBMITTER: Zhang J
PROVIDER: S-EPMC8342216 | biostudies-literature | 2021 Sep
REPOSITORIES: biostudies-literature