scholarly journals Immune Defense Protein Expression in Highly Purified Mouse Lung Epithelial Cells

2016 ◽  
Vol 54 (6) ◽  
pp. 802-813 ◽  
Author(s):  
Meenal Sinha ◽  
Clifford A. Lowell
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Immune Defense ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Defense Protein

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.

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

scholarly journals MAPK signaling pathways regulate IL-8 mRNA stability and IL-8 protein expression in cystic fibrosis lung epithelial cell lines

2011 ◽  
Vol 300 (1) ◽  
pp. L81-L87 ◽  
Author(s):  
Sharmistha Bhattacharyya ◽  
Usha Gutti ◽  
Jose Mercado ◽  
Chad Moore ◽  
Harvey B. Pollard ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Mrna Stability ◽  
Mapk Signaling ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
The Stability ◽  
Mapk Signaling Pathways

Cystic fibrosis (CF) is characterized by a massive proinflammatory phenotype in the lung, caused by mutations in the CFTR gene. IL-8 and other proinflammatory mediators are elevated in the CF airway, and the immediate mechanism may depend on disease-specific stabilization of IL-8 mRNA in CF lung epithelial cells. MAPK signaling pathways impact directly on IL-8 protein expression in CF cells, and we have hypothesized that the mechanism may also involve stabilization of the IL-8 mRNA. To test this hypothesis, we have examined the effects of pharmacological and molecular inhibitors of p38, and downstream MK2, ERK1/2, and JNK, on stability of IL-8 mRNA in CF lung epithelial cells. We previously showed that tristetraprolin (TTP) was constitutively low in CF and that raising TTP destabilized the IL-8 mRNA. We therefore also tested these effects on CF lung epithelial cells stably expressing TTP. TTP binds to AU-rich elements in the 3′-UTR of the IL-8 mRNA. We find that inhibition of p38 and ERK1/2 reduces the stability of IL-8 mRNA in parental CF cells. However, neither intervention further lowers TTP-dependent destabilization of IL-8 mRNA. By contrast, inhibition of the JNK-2 pathway has no effect on IL-8 mRNA stability in parental CF cell, but rather increases the stability of the message in cells expressing high levels of TTP. However, we find that inhibition of ERK1/2 or p38 leads to suppression of the effect of JNK-2 inhibition on IL-8 mRNA stability. These data thus lend support to our hypothesis that constitutive MAPK signaling and proteasomal activity might also contribute, along with aberrantly lower TTP, to the proinflammatory phenotype in CF lung epithelial cells by increasing IL-8 mRNA stability and IL-8 protein expression.

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

scholarly journals Amphiphilic polymer-coated CdSe/ZnS quantum dots induce pro-inflammatory cytokine expression in mouse lung epithelial cells and macrophages

2014 ◽  
Vol 9 (3) ◽  
pp. 336-343 ◽  
Author(s):  
Vivian Lee ◽  
Ryan S. McMahan ◽  
Xiaoge Hu ◽  
Xiaohu Gao ◽  
Elaine M. Faustman ◽  
...  
Keyword(s):  
Quantum Dots ◽  
Epithelial Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Amphiphilic Polymer ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial
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