The probable roles of valsartan in alleviating chronic obstructive pulmonary disease following co-exposure to cold stress and fine particulate matter

Liu, Jiangtao; Lei, Guo; Zhang, Kai; Song, Quanquan; Wei, Qiaozhen; Bian, Qin; Liang, Tingting; Niu, Jingping; Luo, Bin

doi:10.1016/j.etap.2018.05.002

Environmental Toxicology and Pharmacology

2018

DOI: 10.1016/j.etap.2018.05.002

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The probable roles of valsartan in alleviating chronic obstructive pulmonary disease following co-exposure to cold stress and fine particulate matter

Jiangtao Liu

Guo Lei

Kai Zhang

et al.

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Cited by 2 publications

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<p>Fine-particulate matter aggravates cigarette smoke extract–induced airway inflammation via Wnt5a–ERK pathway in COPD</p>

Wang

Zhao²,

Wang³

et al. 2019

COPD

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Background Exposure to environmental particulate matter (PM) ≤2.5 μm in diameter (PM 2.5 ) and smoking are common contributors to COPD, and pertinent research implicates both factors in pulmonary inflammation. Using in vivo mouse and in vitro human cellular models, we investigated the joint impact of PM 2.5 pollution, and cigarette smoke (CS) in mice or cigarette-smoke extract (CSE) in cells on COPD inflammation, and explored potential mechanisms. Methods Tissue changes in lungs of C57BL/6 mice exposed to PM 2.5 and CS were studied by light microscopy, H&E, immunochemistry, and immunofluorescence-stained sections. Levels of inflammatory factors induced by PM 2.5 /CS in mice and PM 2.5 /CSE in 16HBE cells were also monitored by quantitative reverse-transcription (qRT)-PCR and ELISA. Expression of genes related to the Wnt5a-signaling pathway was assessed at transcriptional and protein levels using immunofluorescence, qRT-PCR, and Western blotting. Results Inflammatory response to combined exposure of PM 2.5 and CS or CSE in mouse and 16HBE cells surpassed responses incited separately. Although separate PM 2.5 and CS/CSE exposure upregulated the expression of Wnt5a (a member of the Wnt-secreted glycoprotein family), combined PM 2.5 and CS/CSE exposure produced a steeper rise in Wnt5a levels. Use of a Wnt5a antagonist (BOX5) successfully blocked related inflammatory effects. ERK phosphorylation appeared to mediate the effects of Wnt5a in the COPD model, promoting PM 2.5 aggravation of CS/CSE-induced airway inflammation. Conclusion Our findings suggest that combined PM 2.5 and CS/CSE exposure induce airway inflammation and Wnt5a expression in vivo in mice and in vitro in 16HBE cells. Furthermore, PM 2.5 seems to aggravate CS/CSE-induced inflammation via the Wnt5a–ERK pathway in the context of COPD.

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<p>Fine-particulate matter aggravates cigarette smoke extract–induced airway inflammation via Wnt5a–ERK pathway in COPD</p>

Wang

Zhao²,

Wang³

et al. 2019

COPD

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Implications of DNA damage in chronic lung disease

Zhang,

Sun,

Bao

et al. 2024

Front. Cell Dev. Biol.

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DNA plays an indispensable role in ensuring the perpetuation of life and safeguarding the genetic stability of living organisms. The emergence of diseases linked to a wide spectrum of responses to DNA damage has garnered increasing attention within the scientific community. There is growing evidence that patterns of DNA damage response in the lungs are associated with the onset, progression, and treatment of chronic lung diseases such as chronic obstructive pulmonary disease (COPD), asthma, and bronchopulmonary dysplasia (BPD). Currently, some studies have analyzed the mechanisms by which environmental factors induce lung DNA damage. In this article, we summarize inducible factors of lung DNA damage, current indicators, and methods for diagnosing DNA damage in chronic lung diseases and explore repair mechanisms after DNA damage including nonhomologous end-joining and homology-directed repair end joining pathways. Additionally, drug treatments that may reduce DNA damage or promote repair after it occurs in the lungs are briefly described. In general, more accurate assessment of the degree of lung DNA damage caused by various factors is needed to further elucidate the mechanism of lung DNA damage and repair after damage, so as to search for potential therapeutic targets.

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The probable roles of valsartan in alleviating chronic obstructive pulmonary disease following co-exposure to cold stress and fine particulate matter

Cited by 2 publications

References 40 publications

<p>Fine-particulate matter aggravates cigarette smoke extract–induced airway inflammation via Wnt5a–ERK pathway in COPD</p>

<p>Fine-particulate matter aggravates cigarette smoke extract–induced airway inflammation via Wnt5a–ERK pathway in COPD</p>

Implications of DNA damage in chronic lung disease

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