| Autor: |
Yang, Junxia1 (AUTHOR), Yuan, Yaping1 (AUTHOR), Wang, Linxuan1 (AUTHOR), Deng, Guoping1 (AUTHOR), Huang, Jiaru1 (AUTHOR), Liu, Yuan1 (AUTHOR), Gu, Wenchao1 (AUTHOR) shglsarah@126.com |
| Předmět: |
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| Zdroj: |
Environmental Toxicology. May2024, Vol. 39 Issue 5, p2634-2641. 8p. |
| Abstrakt: |
Background: Chronic obstructive pulmonary disease (COPD) is a widespread inflammatory disease with a high mortality rate. Long noncoding RNAs play important roles in pulmonary diseases and are potential targets for inflammation intervention. Methods: The expression of small nucleolar RNA host gene 6 (SNHG6) in mouse lung epithelial cell line MLE12 with or without cigarette smoke extract (CSE) treatment was first detected using quantitative reverse‐transcription PCR. ELISA was used to evaluate the release of inflammatory cytokines (TNF‐α, IL‐1β, and IL‐6). The binding site of miR‐182‐5p with SNHG6 was predicted by using miRanda, which was verified by double luciferase reporter assay. Results: Here, we revealed that SNHG6 was upregulated in CS‐exposed MLE12 alveolar epithelial cells and lungs from COPD‐model mice. SNHG6 silencing weakened CS‐induced inflammation in MLE12 cells and mouse lungs. Mechanistic investigations revealed that SNHG6 could upregulate IκBα kinase through sponging the microRNA miR‐182‐5p, followed by activated NF‐κB signaling. The suppressive effects of SNHG6 silencing on CS‐induced inflammation were blocked by an miR‐182‐5p inhibitor. Conclusion: Overall, our findings suggested that SNHG6 regulates CS‐induced inflammation in COPD by activating NF‐κB signaling, thereby offering a novel potential target for COPD treatment. [ABSTRACT FROM AUTHOR] |
| Databáze: |
GreenFILE |
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