Induction of Retinoblastoma Gene Expression during Terminal Growth Arrest of a Conditionally Immortalized Fetal Rat Lung Epithelial Cell Line and during Fetal Lung Maturation

1998 ◽  
Vol 239 (2) ◽  
pp. 264-276 ◽  
Author(s):  
R.A. Levine ◽  
T. Hopman ◽  
L. Guo ◽  
M-J. Chang ◽  
N. Johnson
Keyword(s):  
Growth Arrest ◽  
Fetal Lung ◽  
Epithelial Cell Line ◽  
Retinoblastoma Gene ◽  
Rat Lung ◽  
Lung Maturation ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Fetal Rat Lung ◽  
Fetal Lung Maturation

Fetal rat lung maturation: initiation and modulation

1983 ◽  
Vol 55 (6) ◽  
pp. 1725-1732 ◽  
Author(s):  
I. Gross ◽  
C. M. Wilson
Keyword(s):  
Gestational Age ◽  
Fetal Lung ◽  
Defined Medium ◽  
Rat Lung ◽  
Lung Maturation ◽  
Choline Incorporation ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Morphological Maturation ◽  
Fetal Lung Maturation

The purpose of this study was to determine whether a rise in the level of circulating hormones is responsible for initiating fetal lung maturation. Explants of 13- to 20-day fetal rat lung were cultured in a constant chemically defined medium containing 0 or 1% serum. Growth, morphological maturation, and two biochemical markers of lung development, disaturated phosphatidylcholine (DSPC) synthesis and specific nuclear glucocorticoid binding, showed evidence of continuing development in culture. There is normally a marked increase in DSPC content and in the rate of choline incorporation into DSPC after 20 days gestation. Regardless of the gestational age of the fetal lungs used, there was a similar increase in culture at an equivalent gestational age of 20 days (e.g., 14-day lung after 6 days, 16-day lung after 4 days). Removal of 50 or 75% of the lung mesenchymal tissue at the initiation of the culture period did not prevent the increase in choline incorporation. Since the culture environment was constant and contained virtually no hormones, we conclude that the stimulus for the initiation of fetal lung maturation is most likely located in the lung tissue itself. The role of circulating hormones is probably later modulation of the maturational process.

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.

Modeling Glucocorticoid-Mediated Fetal Lung Maturation: II. Temporal Patterns of Gene Expression in Fetal Rat Lung

2005 ◽  
Vol 317 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Mahesh N. Samtani ◽  
Nancy A. Pyszczynski ◽  
Debra C. DuBois ◽  
Richard R. Almon ◽  
William J. Jusko
Keyword(s):  
Gene Expression ◽  
Temporal Patterns ◽  
Fetal Lung ◽  
Rat Lung ◽  
Lung Maturation ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Fetal Lung Maturation

Sex hormones regulate CFTR in developing fetal rat lung epithelial cells

1997 ◽  
Vol 272 (5) ◽  
pp. L844-L851 ◽  
Author(s):  
N. B. Sweezey ◽  
F. Ghibu ◽  
S. Gagnon
Keyword(s):  
Epithelial Cells ◽  
Sex Hormones ◽  
Functional Activity ◽  
Lung Development ◽  
Fetal Lung ◽  
Lung Epithelial Cells ◽  
Rat Lung ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Fetal Rat Lung

Sex hormones modulate two normal processes of late-gestation mammalian lung development: the onset of augmented production of surfactant phospholipids and the loss of mesenchymal cells. As prenatal lung development advances, epithelial chloride secretory pathways diminish as opposing sodium absorptive pathways increase in expression. We hypothesized that sex hormones may influence both the gene expression and functional activity of the chloride channel known as the cystic fibrosis transmembrane conductance regulator (CFTR) in fetal lung epithelium. We report here that sex hormones exert opposite effects on CFTR. Androgen increases and estrogen decreases CFTR functional activity [as assessed by CFTR antisense (but not sense) oligodeoxynucleotide-sensitive adenosine 3',5'-cyclic monophosphate-stimulated cell volume reduction or by glibenclamide-sensitive, amiloride-insensitive transepithelial electrical potential] in primary cultures of fetal rat lung epithelial cells. No alterations in CFTR mRNA levels measured by quantitative polymerase chain reaction amplification of reverse transcripts) accompanied either the changes in functional activity induced by sex hormones or the changes observed during normal development, suggesting that sex hormone modulation of CFTR in antenatal lung occurs at a posttranscriptional level. Our data are consistent with the hypothesis that both androgen and estrogen contribute to the male disadvantage with respect to fetal lung functional development.

Growth of distal fetal rat lung epithelial cells in a defined serum-free medium

1991 ◽  
Vol 27 (8) ◽  
pp. 625-632 ◽  
Author(s):  
D. Jassal ◽  
R. N. N. Han ◽  
I. Caniggia ◽  
M. Post ◽  
A. K. Tanswell
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Rat Lung ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Fetal Rat Lung

scholarly journals Fetal rat lung epithelium has a functional growth hormone receptor coupled to tyrosine kinase activity and insulin-like growth factor binding protein-2 production

1998 ◽  
Vol 21 (1) ◽  
pp. 73-84 ◽  
Author(s):  
DC Batchelor ◽  
RM Lewis ◽  
BH Breier ◽  
PD Gluckman ◽  
SJ Skinner
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Binding Protein ◽  
Fetal Lung ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Rat Lung ◽  
Lung Epithelium ◽  
Fetal Rat ◽  
Fetal Rat Lung

Although growth hormone (GH) receptor (GHR) mRNA and protein are present in fetal tissues such as the lung, there is little evidence that GH mediates growth in the fetus. We have identified functional responses to GH in fetal rat lung epithelia and suggest a possible role for GHR in the developing lung. GHR mRNA in lung extracts was high before birth at day 16 of gestation (16f), decreased to low levels at day 22f but increased again after birth. At day 20f GHR mRNA levels were higher in lung than in liver, whereas growth hormone binding protein mRNA levels were approximately equal in lung and liver. Stimulation of primary cell cultures of day 19f lung epithelia with GH caused increased tyrosine phosphorylation in specific proteins, demonstrating functional GHR. Lung fibroblasts isolated at the same time did not respond to GH. Ligand and Northern blot analysis of the epithelial cultures revealed that GH stimulation increased insulin-like growth factor binding protein-2 (IGFBP-2) activity and mRNA. These experiments demonstrate the functional activity of GHR, specifically in fetal lung epithelium. We suggest that one role for GH in vivo may be indirectly to modify insulin-like growth factor activity in the developing fetal lung by increasing IGFBP-2.

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