Lnc-IL7R alleviates PM2.5-mediated cellular senescence and apoptosis through EZH2 recruitment in chronic obstructive pulmonary disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2022-03-18

AUTHORS

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

ABSTRACT

BackgroundLong-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.MethodsAssociations 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.ResultsLnc-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.ConclusionLnc-IL7R attenuates PM2.5-mediated p21CIP1/WAF1 expression through EZH2 recruitment, and its dysfunction may augment cellular injury in COPD.Graphical abstract More... »

PAGES

1-24

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10565-022-09709-1

DOI

http://dx.doi.org/10.1007/s10565-022-09709-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1146380144

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/35303175


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