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| 題名: | Lnc-IL7R alleviates PM2.5-mediated cellular senescence and apoptosis through EZH2 recruitment in chronic obstructive pulmonary disease |
| 作者: | 吳聲明
Kang-Yun Lee, Shu-Chuan Ho, Wei-Lun Sun, Po-Hao Feng, Cheng-Wei Lin, Kuan-Yuan Chen, Hsiao-Chi Chuang, Chien-Hua Tseng, Tzu-Tao Chen, Sheng-Ming Wu |
| 貢獻者: | 醫學系內科學科胸腔內科 |
| 關鍵詞: | Keywords: COPD;Emphysema;Lnc-IL7R;PM2.5;Senescence |
| 日期: | 2022-12 |
| 上傳時間: | 2025-03-31 09:13:55 (UTC+8) |
| 摘要: | Abstract
Background: Long-term exposure to PM2.5 (particulate matter with an aerodynamic diameter of ? 2.5 μm) is associated with pulmonary injury and emphysema in patients with chronic obstructive pulmonary disease (COPD). We investigated mechanisms through which the long noncoding RNA lnc-IL7R contributes to cellular damage by inducing oxidative stress in COPD patients exposed to PM2.5.
Methods: Associations of serum lnc-IL7R levels with lung function, emphysema, and previous PM2.5 exposure in COPD patients were analyzed. Reactive oxygen species and lnc-IL7R levels were measured in PM2.5-treated cells. The levels of lnc-IL7R and cellular senescence-associated genes, namely p16INK4a and p21CIP1/WAF1, were determined through lung tissue section staining. The effects of p16INK4a or p21CIP1/WAF1 regulation were examined by performing lnc-IL7R overexpression and knockdown assays. The functions of lnc-IL7R-mediated cell proliferation, cell cycle, senescence, colony formation, and apoptosis were examined in cells treated with PM2.5. Chromatin immunoprecipitation assays were conducted to investigate the epigenetic regulation of p21CIP1/WAF1.
Results: Lnc-IL7R levels decreased in COPD patients and were negatively correlated with emphysema or PM2.5 exposure. Lnc-IL7R levels were upregulated in normal lung epithelial cells but not in COPD cells exposed to PM2.5. Lower lnc-IL7R expression in PM2.5-treated cells induced p16INK4a and p21CIP1/WAF1 expression by increasing oxidative stress. Higher lnc-IL7R expression protected against cellular senescence and apoptosis, whereas lower lnc-IL7R expression augmented injury in PM2.5-treated cells. Lnc-IL7R and the enhancer of zeste homolog 2 (EZH2) synergistically suppressed p21CIP1/WAF1 expression through epigenetic modulation.
Conclusion: Lnc-IL7R attenuates PM2.5-mediated p21CIP1/WAF1 expression through EZH2 recruitment, and its dysfunction may augment cellular injury in COPD. |
| 關聯: | Cell Biol Toxicol. 2022 Dec; 38(6): 1097-1120 |
| 描述: | 【111-1 升等】臺北醫學大學教師升等專門著作
職別：專任教師
送審等級：副教授
著作送審 |
| 資料類型: | article |
| 顯示於類別: | [教師升等送審著作] 111
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