Stretch-Induced Growth-Promoting Activities Stimulate Fetal Rat Lung Epithelial Cell Proliferation

1993 ◽  
Vol 19 (4) ◽  
pp. 505-517 ◽  
Author(s):  
Mingyao Liu ◽  
Jing Xu ◽  
A. Keith Tanswell ◽  
Martin Post
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Lung Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Rat Lung ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Fetal Rat Lung ◽  
Growth Promoting

Spatial and temporal differences in fibroblast behavior in fetal rat lung

1991 ◽  
Vol 261 (6) ◽  
pp. L424-L433 ◽  
Author(s):  
I. Caniggia ◽  
I. Tseu ◽  
R. N. Han ◽  
B. T. Smith ◽  
K. Tanswell ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Lung Development ◽  
Epithelial Cell Proliferation ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Growth Promoting ◽  
In Cells

Fibroblast-epithelial interactions were investigated in cells from late-gestation fetal rat lung. Fibroblasts from the pseudoglandular stage of lung development stimulated epithelial cell proliferation, whereas fibroblasts from the saccular stage promoted epithelial cell differentiation. The developmental switch from proliferation to differentiation seemed to be controlled by both cell types. Fibroblast-derived epithelial cell growth-promoting activity, evident in cells from the pseudoglandular period, decreased during development and almost disappeared in cells from the saccular stage. Interestingly, the response of epithelial cells to this growth-promoting activity declined with advancing gestational age as epithelial cells became more responsive to fibroblast-derived differentiation factor(s). Production of differentiation factor(s) by fibroblasts increased during the canalicular stage of lung development. Platelet-derived growth factor (PDGF) and low concentrations of transforming growth factor-beta (TGF-beta) stimulated epithelial cell proliferation. PDGF did not affect differentiation, whereas TGF-beta was inhibitory. Dependent on their proximity to the epithelium, two subpopulations of fibroblasts that differed in their ability to promote epithelial cell proliferation or differentiation were isolated. Fibroblasts in close proximity to the epithelium mainly produced differentiation factors, whereas more distant fibroblasts primarily stimulated proliferation.

Na+-K+-ATPase gene regulation by glucocorticoids in a fetal lung epithelial cell line

1999 ◽  
Vol 277 (1) ◽  
pp. L197-L203 ◽  
Author(s):  
Sridar Chalaka ◽  
David H. Ingbar ◽  
Renuka Sharma ◽  
Zhong Zhau ◽  
Christine H. Wendt
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Fetal Lung ◽  
Lung Epithelial Cell ◽  
Epithelial Cell Line ◽  
Rat Lung ◽  
Fetal Rat ◽  
Atpase Gene ◽  
Lung Epithelial ◽  
Fetal Rat Lung

The Na+pump, Na+-K+-ATPase, along with the Na+channel is essential for the removal of alveolar solute and fluid perinatally. Because Na+-pump mRNA and activity increase before birth and maternal glucocorticoids (GCs) influence Na+-K+-ATPase mRNA expression in fetal rat lung, we hypothesized that GCs increased Na+-K+-ATPase gene expression in a fetal lung epithelial cell line. After 24 h of exposure, dexamethasone increased the steady-state levels of Na+-K+-ATPase α1and β1mRNA in a fetal rat lung epithelial cell line in a dose-dependent fashion (10−7to 10−5M). The maximal increase in mRNA levels was 3.8-fold for α1and 2.8-fold for β1. The increase in mRNA was detected as early as 6 h for the β1-subunit and 18 h for the α1-subunit, and both peaked at 24 h. This gene upregulation was not due to increased mRNA stability based on mRNA half-life determination after actinomycin D inhibition. Transfection experiments with α1and β1promoter-reporter constructs demonstrated 3.2 ± 0.5- and 2.6 ± 0.4-fold increases, respectively, in promoter activity, consistent with transcriptional activation of the promoter-reporter construct. These findings, increased promoter activity with no change in stability, indicate that GCs increased Na+-K+-ATPase transcription in a fetal lung epithelial cell line.

scholarly journals The LIM-domain only protein 4 contributes to lung epithelial cell proliferation but is not essential for tumor progression

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Aliaksei Z. Holik ◽  
Caitlin E. Filby ◽  
Julie Pasquet ◽  
Kati Viitaniemi ◽  
John Ciciulla ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Tumor Progression ◽  
Lung Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Lim Domain ◽  
Lung Epithelial

scholarly journals SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNγ-Induced Antiviral Gene Expression in Human Lung Epithelial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Hua Geng ◽  
Saravanan Subramanian ◽  
Longtao Wu ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Viral Infection ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial Cell ◽  
Accessory Protein ◽  
Epithelial Cell Proliferation ◽  
Lung Epithelial

Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a disease that involves significant lung tissue damage. How SARS-CoV-2 infection leads to lung injury remains elusive. The open reading frame 8 (ORF8) protein of SARS-CoV-2 (ORF8SARS-CoV-2) is a unique accessory protein, yet little is known about its cellular function. We examined the cellular distribution of ORF8SARS-CoV-2 and its role in the regulation of human lung epithelial cell proliferation and antiviral immunity. Using live imaging and immunofluorescent staining analyses, we found that ectopically expressed ORF8SARS-CoV-2 forms aggregates in the cytosol and nuclear compartments of lung epithelial cells. Using in silico bioinformatic analysis, we found that ORF8SARS-CoV-2 possesses an intrinsic aggregation characteristic at its N-terminal residues 1-18. Cell culture did not reveal any effects of ORF8SARS-CoV-2 expression on lung epithelial cell proliferation and cell cycle progression, suggesting that ORF8SARS-CoV-2 aggregates do not affect these cellular processes. Interestingly, ectopic expression of ORF8SARS-CoV-2 in lung epithelial cells suppressed basal expression of several antiviral molecules, including DHX58, ZBP1, MX1, and MX2. In addition, expression of ORF8SARS-CoV-2 attenuated the induction of antiviral molecules by IFNγ but not by IFNβ in lung epithelial cells. Taken together, ORF8SARS-CoV-2 is a unique viral accessory protein that forms aggregates when expressing in lung epithelial cells. It potently inhibits the expression of lung cellular anti-viral proteins at baseline and in response to IFNγ in lung epithelial cells, which may facilitate SARS-CoV-2 escape from the host antiviral innate immune response during early viral infection. In addition, it seems that formation of ORF8SARS-CoV-2 aggregate is independent from the viral infection. Thus, it would be interesting to examine whether any COVID-19 patients exhibit persistent ORF8 SARS-CoV-2 expression after recovering from SARS-CoV-2 infection. If so, the pathogenic effect of prolonged ORF8SARS-CoV-2 expression and its association with post-COVID symptoms warrant investigation in the future.

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