Murine lung response to kaolin conveyed by cigarette smoke

1988 ◽  
Vol 413 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Daniel H. Matulionis ◽  
obert A. Yokel
Keyword(s):  
Cigarette Smoke ◽  
Murine Lung ◽  
Lung Response

Effect Of Cigarette Smoke Extract Or TGF-Beta1 On Hyaluronan Production And Hyaluronan Modulating Enzymes In Primary Murine Lung Fibroblasts

2011 ◽  
Author(s):  
Ken R. Bracke ◽  
Juanita H. Vernooy ◽  
Tine Demoor ◽  
Guy F. Joos ◽  
Emiel F. Wouters ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Lung Fibroblasts ◽  
Murine Lung

Cigarette Smoke Exposure Reduces The Deposition And Activity Of Extracellular Superoxide Dismutase In Murine Lung

2011 ◽  
Author(s):  
Hataya K. Poonyagariyagorn ◽  
Shana Metzger ◽  
Kaori Misono ◽  
Kavita Sapru ◽  
Armando Lopez-Mercado ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Extracellular Superoxide Dismutase ◽  
Murine Lung

Cigarette Smoke Exposure Increases Mast Cells and mMCP-1 in the Murine Lung.

2009 ◽  
Author(s):  
JK Nikota ◽  
FM Botelho ◽  
NJ Trimble ◽  
AJ Coyle ◽  
R Kolbeck ◽  
...  
Keyword(s):  
Mast Cells ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Murine Lung

Cigarette smoke inhalation: Effects on cells of the immune series in the murine lung

Life Sciences ◽  
1973 ◽  
Vol 12 (8) ◽  
pp. 377-383 ◽  
Author(s):  
Patrick G. Holt ◽  
David Keast
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Murine Lung

Aberrant Promoter Hypermethylation of the Death-Associated Protein Kinase Gene Is Early and Frequent in Murine Lung Tumors Induced by Cigarette Smoke and Tobacco Carcinogens

2004 ◽  
Vol 64 (11) ◽  
pp. 3844-3848 ◽  
Author(s):  
Leah C. Pulling ◽  
Brian R. Vuillemenot ◽  
Julie A. Hutt ◽  
Theodora R. Devereux ◽  
Steven A. Belinsky
Keyword(s):  
Protein Kinase ◽  
Cigarette Smoke ◽  
Promoter Hypermethylation ◽  
Lung Tumors ◽  
Kinase Gene ◽  
Murine Lung ◽  
Death Associated Protein Kinase ◽  
Protein Kinase Gene ◽  
Tobacco Carcinogens

scholarly journals Regional Heterogeneity in Murine Lung Fibroblasts from Normal Mice or Mice Exposed Once to Cigarette Smoke

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39761 ◽  
Author(s):  
Olena Preobrazhenska ◽  
Joanne L. Wright ◽  
Andrew Churg
Keyword(s):  
Cigarette Smoke ◽  
Lung Fibroblasts ◽  
Regional Heterogeneity ◽  
Murine Lung

scholarly journals E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells

2018 ◽  
Vol 115 (7) ◽  
pp. E1560-E1569 ◽  
Author(s):  
Hyun-Wook Lee ◽  
Sung-Hyun Park ◽  
Mao-wen Weng ◽  
Hsiang-Tsui Wang ◽  
William C. Huang ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Human Lung ◽  
Mouse Lung ◽  
Urothelial Cells ◽  
Bronchial Epithelial ◽  
Murine Lung ◽  
Repair Activity ◽  
Tumorigenic Transformation ◽  
Bladder Cells

E-cigarette smoke delivers stimulant nicotine as aerosol without tobacco or the burning process. It contains neither carcinogenic incomplete combustion byproducts nor tobacco nitrosamines, the nicotine nitrosation products. E-cigarettes are promoted as safe and have gained significant popularity. In this study, instead of detecting nitrosamines, we directly measured DNA damage induced by nitrosamines in different organs of E-cigarette smoke-exposed mice. We found mutagenic O6-methyldeoxyguanosines and γ-hydroxy-1,N2-propano-deoxyguanosines in the lung, bladder, and heart. DNA-repair activity and repair proteins XPC and OGG1/2 are significantly reduced in the lung. We found that nicotine and its metabolite, nicotine-derived nitrosamine ketone, can induce the same effects and enhance mutational susceptibility and tumorigenic transformation of cultured human bronchial epithelial and urothelial cells. These results indicate that nicotine nitrosation occurs in vivo in mice and that E-cigarette smoke is carcinogenic to the murine lung and bladder and harmful to the murine heart. It is therefore possible that E-cigarette smoke may contribute to lung and bladder cancer, as well as heart disease, in humans.

scholarly journals DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease

2015 ◽  
Vol 309 (10) ◽  
pp. L1124-L1137 ◽  
Author(s):  
Jodie Birch ◽  
Rhys K. Anderson ◽  
Clara Correia-Melo ◽  
Diana Jurk ◽  
Graeme Hewitt ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Cigarette Smoke Exposure ◽  
Telomere Dysfunction ◽  
Airway Epithelial ◽  
Murine Lung ◽  
Small Airway Epithelial Cells ◽  
Lung Aging

Cellular senescence has been associated with the structural and functional decline observed during physiological lung aging and in chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the first line of defense in the lungs and are important to COPD pathogenesis. However, the mechanisms underlying airway epithelial cell senescence, and particularly the role of telomere dysfunction in this process, are poorly understood. We aimed to investigate telomere dysfunction in airway epithelial cells from patients with COPD, in the aging murine lung and following cigarette smoke exposure. We evaluated colocalization of γ-histone protein 2A.X and telomeres and telomere length in small airway epithelial cells from patients with COPD, during murine lung aging, and following cigarette smoke exposure in vivo and in vitro. We found that telomere-associated DNA damage foci increase in small airway epithelial cells from patients with COPD, without significant telomere shortening detected. With age, telomere-associated foci increase in small airway epithelial cells of the murine lung, which is accelerated by cigarette smoke exposure. Moreover, telomere-associated foci predict age-dependent emphysema, and late-generation Terc null mice, which harbor dysfunctional telomeres, show early-onset emphysema. We found that cigarette smoke accelerates telomere dysfunction via reactive oxygen species in vitro and may be associated with ataxia telangiectasia mutated-dependent secretion of inflammatory cytokines interleukin-6 and -8. We propose that telomeres are highly sensitive to cigarette smoke-induced damage, and telomere dysfunction may underlie decline of lung function observed during aging and in COPD.

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