Glucocorticoid receptor mRNA and protein in fetal rat lung in vivo: modulation by glucocorticoid and androgen

1998 ◽  
Vol 275 (1) ◽  
pp. L103-L109 ◽  
Author(s):  
Neil B. Sweezey ◽  
F. Ghibu ◽  
S. Gagnon ◽  
E. Schotman ◽  
Q. Hamid
Keyword(s):  
Glucocorticoid Receptor ◽  
Primary Culture ◽  
Lung Development ◽  
Fetal Lung ◽  
Lung Cells ◽  
Human Antibody ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

Pulmonary glucocorticoid receptor (GR) is essential to timely preparation for the onset of breathing air at birth. We have previously used primary culture of late-gestation fetal rat lung cells to demonstrate differential regulation of GR by glucocorticoid depending on cell type. In this study, we hypothesized that the action of glucocorticoid on GR mRNA expression and protein elaboration in lung cells might be modulated by interactions present in vivo but not in primary culture. Given that male sex hormone (androgen) has an inhibitory effect on antenatal lung development, we also postulated that androgen would decrease antenatal lung GR. We report that antenatal maternal injection of the glucocorticoid dexamethasone (1 mg/kg) enhanced fetal lung cellular levels of GR mRNA and protein as assessed by in situ hybridization and immunocytochemistry (ICC), respectively. ICC was performed using polyclonal rabbit anti-human antibody that reacts with rat GR whether bound to ligand or not and does not interfere with GR binding to DNA. Levels of GR mRNA and protein were enhanced in cells throughout all areas of the lung tissue, suggesting that interactions occurring in intact tissue may override the previously reported direct inhibition by glucocorticoid of GR protein elaboration in isolated fetal rat lung epithelial cells. Furthermore, antenatal administration of the androgen 5α-dihydrotestosterone (0.2 mg/kg) reduced tissue levels of GR mRNA and protein, consistent with androgenic inhibition of antenatal lung development by decreasing GR. We conclude that glucocorticoids and androgens exert opposite effects on fetal lung GR.

An Ultrastructural Comparison of Rat Lung Cells Grown in an Organotypic Culture System with Lung Tissue Found in the Whole Animal

1976 ◽  
Vol 34 ◽  
pp. 172-173
Author(s):  
Peter J. Del Vecchio ◽  
Edward P. Dougherty ◽  
William H. J. Douglas
Keyword(s):  
Lung Tissue ◽  
Organotypic Culture ◽  
Fetal Lung ◽  
Lung Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Tissue Organization ◽  
Fetal Rat ◽  
Fetal Rat Lung

This study describes the ultrastructure of an organotypic system prepared from rat fetal lung and compares it to lung in rat fetuses. The preparation of the organotypic system has been described elsewhere (1).The organotypic systems in this study are prepared from 18-19 day fetal rat lung and spend two days in culture making the cells a total of 20-21 days old. The fine structure of the type II cells present in this system will be compared to the type II cells in fetal lung at 20-21 days gestation. Because the tissue organization of the organotypic system is more like the organization of fetal lung at an earlier stage (18-19 days gestation) , the cell to cell relationships of the organotypic system are compared to fetal lung tissue at this stage.The histology of the organotypic system is similar to that of the fetal lung in its glandular stage (Fig. 1). The epithelial cells are all columnar and are surrounded by relatively undifferentiated mesenchyme.

Growth and developmental regulation of wnt-2 (irp) gene in mesenchymal cells of fetal lung

1992 ◽  
Vol 262 (6) ◽  
pp. L672-L683 ◽  
Author(s):  
B. K. Levay-Young ◽  
M. Navre
Keyword(s):  
Lung Development ◽  
Developmental Regulation ◽  
Fetal Lung ◽  
Fibroblast Cell ◽  
Mrna Levels ◽  
Rat Lung ◽  
Intercellular Interaction ◽  
Wnt Proteins ◽  
Fetal Rat ◽  
Fetal Rat Lung

The wnt gene family encodes a group of proteins implicated as intercellular signaling molecules in vertebrate development. Because many wnt genes are also expressed in the lung, we have examined whether the wnt family member wnt-2 (irp) plays a role in lung development. We have cloned rat wnt-2 and found that this cDNA detects multiple mRNAs expressed at high levels in fetal rat lung. Much lower levels were found in adult rat lung and other tissues, including, surprisingly, the mammary gland. The wnt-2 mRNA was also detected in human fetal lung fibroblast cell lines, where the mRNA levels were dramatically regulated by growth state as well as growth factor stimulation. In situ hybridization showed that, in fetal rat lung, wnt-2 mRNA expression is restricted to the mesenchyme; levels in the developing epithelium were indistinguishable from background. Based on the known properties of other wnt proteins, our data lead us to propose that wnt-2 may play a role in lung development by mediating intercellular interaction(s) between mesenchyme and epithelium.

scholarly journals Differential Regulation of Glucocorticoid Receptor Expression by Ligand in Fetal Rat Lung Cells

1995 ◽  
Vol 38 (4) ◽  
pp. 506-512 ◽  
Author(s):  
Neil Sweezey ◽  
Carolyn Mawdsley ◽  
Felicia Ghibu ◽  
Li Song ◽  
Shilpa Buch ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Differential Regulation ◽  
Receptor Expression ◽  
Lung Cells ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

scholarly journals Mechanical strain-induced posttranscriptional regulation of fibronectin production in fetal lung cells

1999 ◽  
Vol 277 (1) ◽  
pp. L142-L149 ◽  
Author(s):  
Eric Mourgeon ◽  
Jing Xu ◽  
A. Keith Tanswell ◽  
Mingyao Liu ◽  
Martin Post
Keyword(s):  
Cell Proliferation ◽  
Mechanical Strain ◽  
Fetal Lung ◽  
Northern Analysis ◽  
Normal Lung ◽  
Lung Cells ◽  
Mrna Levels ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

We have shown that intermittent mechanical strain, simulating fetal breathing movements, stimulated fetal rat lung cell proliferation. Because normal lung growth requires proper coordination between cell proliferation and extracellular matrix remodeling, we investigated the effect of strain on fibronectin metabolism. Organotypic cultures of fetal rat lung cells, subjected to intermittent strain, showed increased fibronectin content in the culture media. Fibronectin-degrading activity in media from strained cells was similar to that of static cultures. Northern analysis revealed that strain inhibited fibronectin mRNA accumulation seen during static culture. Synthesis of fibronectin, determined by metabolic labeling, was increased by strain despite lower mRNA levels or presence of actinomycin D. This increase was not mediated via a rapamycin-sensitive mechanism. Strain stimulated prelabeled fibronectin secretion even in the presence of cycloheximide. These results suggest that strain differentially regulates fibronectin production of fetal lung cells at the transcriptional and posttranscriptional levels. Mechanical strain increases soluble fibronectin content by stimulating its synthesis and secretion without increasing fibronectin message levels.

Differential regulation of extracellular matrix molecules by mechanical strain of fetal lung cells

1999 ◽  
Vol 276 (5) ◽  
pp. L728-L735 ◽  
Author(s):  
Jing Xu ◽  
Mingyao Liu ◽  
Martin Post
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Mechanical Strain ◽  
Fetal Lung ◽  
Lung Cells ◽  
Gelatinase A ◽  
Rat Lung ◽  
Fetal Rat ◽  
Gene And Protein Expression ◽  
Fetal Rat Lung

We have previously shown that an intermittent mechanical strain regimen (5% elongation, 60 cycles/min, 15 min/h) that simulates fetal breathing movements stimulated fetal rat lung cell proliferation. Because normal lung growth requires proper coordination between cell proliferation and extracellular matrix (ECM) remodeling, we subjected organotypic cultures of fetal rat lung cells ( day 19 of gestation, term = 22 days) to this strain regimen and examined alterations in ECM gene and protein expression. Northern analysis revealed that mechanical strain reduced messages for procollagen-α1(I) and biglycan and increased the levels of mRNA for collagen-α1(IV) and -α2(IV), whereas laminin β-chain mRNA levels remained constant. Regardless of mRNA changes, mechanical strain increased the protein content of type I and type IV collagen as well as of biglycan in the medium. Mechanical strain did not affect gene expression of several matrix metalloproteinases (MMPs), such as MMP-1 (interstitial collagenase), MMP-2 (gelatinase A), and MMP-3 (stromelysin-1). Neither collagenase nor gelatinase (A and B) activities in conditioned medium were affected by mechanical strain. Tissue inhibitor of metalloproteinase activities in conditioned medium remained unchanged during the 48-h intermittent mechanical stretching. These data suggest that an intermittent mechanical strain differentially regulates gene and protein expression of ECM molecules in fetal lung cells. The observed increase in matrix accumulation appears to be mainly a result of an increased synthesis of ECM molecules and not of decreasing activity of degradative enzymes.

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.

scholarly journals Influence of Epidermal Growth Factor on Fetal Rat Lung Development in Vitro

1986 ◽  
Vol 20 (5) ◽  
pp. 473-477 ◽  
Author(s):  
Lan Gross ◽  
Diane W Dynia ◽  
Seamus A Rooney ◽  
Douglas A Smart ◽  
Joseph B Warshaw ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Development ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung ◽  
Epidermal Growth ◽  
Development In Vitro

Fetal Rat Lung Development: Lipids and Surface Tension Properties After Decapitation in utero

1972 ◽  
Vol 140 (3) ◽  
pp. 885-889 ◽  
Author(s):  
W. R. Blackburn ◽  
D. M. Potter ◽  
H. Travers ◽  
L. L. Gassenheimer ◽  
R. A. Rhoades
Keyword(s):  
Surface Tension ◽  
Lung Development ◽  
In Utero ◽  
Rat Lung ◽  
Fetal Rat ◽  
Tension Properties ◽  
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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