[1] PubMed ID: | 33791009 |
Disease Name: | Sleep Apnea Syndromes |
Sample: | the adenoids of patients with OSAHS |
Dysfunction Pattern: | Regulation(GRα-NF-κB signaling pathway) |
Validated Method: | RNA Pull-Down//Western Blot//Transfection//qRT-PCR//ELISA//Bioinformatics Analysis |
Description: | Furthermore, reverse transcription-quantitative PCR showed that the expression of lncRNA XIST was significantly increased in the adenoids of patients with OSAHS compared with healthy controls. The stimulatory effect of XIST was significantly inhibited by the NF-κB inhibitor EVP4593. These results indicated that the stimulatory effect of XIST was dependent on NF-κB. In summary, the present study demonstrated that the XIST-GRα-NF-κB signaling pathway contributed to inflammation in the adenoids of patients with OSAHS. |
Causality: | Yes |
Causal Description: | Further in vitro studies by Pearson correlation analysis, RNA pull-down assay, western blot analysis and ELISA demonstrated that XIST significantly decreased the expression of GRα and that significantly increased the production of inflammatory cytokines, including interleukin (IL)-8, tumor necrosis factor α, IL-6 and IL-1β, while the overexpression of GRα significantly decreased the production of these inflammatory cytokines in NP69 cells, a human nasopharyngeal epithelial cell line. Furthermore, XIST significantly increased the protein levels of nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) subunits, including Rel-B, c-Rel, P52, P50 and P65, which are associated with the transcription of cytokines. |
Clinical-realted Application: | |
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