Redox-Dependent Expression of Cyclin D1 and Cell Proliferation by Nox1 in Mouse Lung Epithelial Cells

2006 ◽  
Vol 8 (9-10) ◽  
pp. 1447-1459 ◽  
Author(s):  
Priya Ranjan ◽  
Vikas Anathy ◽  
Peter M. Burch ◽  
Kelly Weirather ◽  
J. David Lambeth ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial

Cyclin D1 as a proliferative marker regulating retinoblastoma phosphorylation in mouse lung epithelial cells

2001 ◽  
Vol 168 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Cynthia L Mamay ◽  
Irene E Schauer ◽  
Pamela L Rice ◽  
Lori D Dwyer-Nield ◽  
Ming You ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclin D1 ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Proliferative Marker

Corrigendum to “Cyclin D1 as a proliferative marker regulating retinoblastoma phosphorylation in mouse lung epithelial cells”

2002 ◽  
Vol 180 (2) ◽  
pp. 223
Author(s):  
Cynthia L. Mamay ◽  
Irene E. Schauer ◽  
Pamela L. Rice ◽  
Amy McDoniels-Silvers ◽  
Lori D. Dwyer-Nield ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclin D1 ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Proliferative Marker

scholarly journals Effect of Slit/Robo signaling on regeneration in lung emphysema

2021 ◽  
Author(s):  
Jin-Soo Park ◽  
RyeonJin Cho ◽  
Eun-Young Kang ◽  
Yeon-Mok Oh
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Chronic Obstructive ◽  
Irreversible Damage ◽  
Lung Epithelial ◽  
And Migration ◽  
Proliferation And Migration

AbstractEmphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.

Carbon nanoparticle-induced lung epithelial cell proliferation is mediated by receptor-dependent Akt activation

2008 ◽  
Vol 294 (2) ◽  
pp. L358-L367 ◽  
Author(s):  
Klaus Unfried ◽  
Ulrich Sydlik ◽  
Katrin Bierhals ◽  
Alexander Weissenberg ◽  
Josef Abel
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Carbon Nanoparticles ◽  
Growth Factor Receptor ◽  
Lung Epithelial Cells ◽  
Alveolar Type ◽  
Specific Cell ◽  
Akt Inhibitor ◽  
Signaling Mechanism ◽  
Lung Epithelial

Treatment of lung epithelial cells with different kinds of nano-sized particles leads to cell proliferation. Because bigger particles fail to induce this reaction, it is suggested that the special surface properties, due to the extremely small size of these kinds of materials, is the common principle responsible for this specific cell reaction. Here the activation of the protein kinase B (Akt) signaling cascade by carbon nanoparticles was investigated with regard to its relevance for proliferation. Kinetics and dose-response experiments demonstrated that Akt is specifically activated by nanoparticulate carbon particles in rat alveolar type II epithelial cells as well as in human bronchial epithelial cells. This pathway appeared to be dependent on epidermal growth factor receptor and β1-integrins. The activation of Akt by these receptors is known to be a feature of adhesion-dependent signaling. However, intracellular proteins described in this context (focal adhesion kinase pp125FAK and integrin-linked kinase) were not activated, indicating a specific signaling mechanism. Inhibitor studies demonstrate that nanoparticle-induced proliferation is mediated by phosphoinositide 3-kinases and Akt. Moreover, overexpression of mutant Akt, as well as pretreatment with an Akt inhibitor, reduced nanoparticle-specific ERK1/2 phosphorylation, which is decisive for nanoparticle-induced proliferation. With this report, we describe the activation of a pathway by carbon nanoparticles that was so far known to be triggered by ligand receptor binding or on cell adhesion to extracellular matrix proteins.

scholarly journals Ex vivo model of non‑small cell lung cancer using mouse lung epithelial cells

2017 ◽  
Author(s):  
Taku Sato ◽  
Mami Morita ◽  
Ryota Tanaka ◽  
Yui Inoue ◽  
Miyuki Nomura ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Small Cell Lung Cancer ◽  
Ex Vivo ◽  
Small Cell ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Small Cell Lung ◽  
Ex Vivo Model ◽  
Lung Epithelial

scholarly journals Selection of rhinovirus 1A variants adapted for growth in mouse lung epithelial cells

Virology ◽  
2011 ◽  
Vol 420 (2) ◽  
pp. 82-88 ◽  
Author(s):  
Angela L. Rasmussen ◽  
Vincent R. Racaniello
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Selection Of
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