Epithelial cell differentiation in organotypic cultures of fetal rat lung

1985 ◽  
Vol 172 (1) ◽  
pp. 31-40 ◽  
Author(s):  
L. L. Simpson ◽  
A. K. Tanswell ◽  
M. G. Joneja
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Rat Lung ◽  
Organotypic Cultures ◽  
Epithelial Cell Differentiation ◽  
Fetal Rat ◽  
Fetal Rat Lung

Effects of the Antiglucocorticoid RU 486 on the Initiation of Ultrastructural Type-II Cell Differentiation in Fetal Rat Lung

Neonatology ◽  
1990 ◽  
Vol 58 (3) ◽  
pp. 173-180 ◽  
Author(s):  
Nadia Guettari ◽  
Marie-Elizabeth Dufour ◽  
Léa Marin
Keyword(s):  
Cell Differentiation ◽  
Type Ii ◽  
Rat Lung ◽  
Ru 486 ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Type Ii Cell

scholarly journals Organotypic cultures of diploid type II alveolar pneumonocytes: surfactant associated esterase activity.

1979 ◽  
Vol 27 (4) ◽  
pp. 852-856 ◽  
Author(s):  
W H Douglas ◽  
K R Hitchcock
Keyword(s):  
Esterase Activity ◽  
Lamellar Body ◽  
Nonspecific Esterase ◽  
Type Ii ◽  
Rat Lung ◽  
Organotypic Cultures ◽  
Surfactant Synthesis ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Nonspecific Esterases

Organotypic cultures, established from enzymatically dispersed day 19 fetal rat lung, are comprised primarily of cells which are morphologically similar to type II alveolar pneumonocytes, the cells involved in surfactant synthesis. To further characterize these cultures, the nonspecific esterase pool was examined to determine if these cultures contained certain nonspecific esterases previously shown to be enzyme markers for the surfactant system. The results of biochemical, electrophoretic and cytochemical studies indicate that these organotypic cultures contain the same nonspecific esterases already demonstrated in surface active fractions derived from rat and mouse lung homogenates and pulmonary lavage fluid. As in whole lung, the major site of esterase activity in the organotypic cultures is the type II cell lamellar body, the putative site of surfactant synthesis and storage. These findings support the concept that the organotypic cultures derived from fetal rat lung are comprised predominantly of type II cells which retain surfactant associated functions in vitro.

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.

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