Morphometric analysis of fetal rat lung development

1993 ◽  
Vol 237 (1) ◽  
pp. 38-48 ◽  
Author(s):  
Michael Moschopulos ◽  
Peter H. Burri
Keyword(s):  
Morphometric Analysis ◽  
Lung Development ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

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

Nitric oxide modulates branching morphogenesis in fetal rat lung explants

2002 ◽  
Vol 282 (3) ◽  
pp. L379-L385 ◽  
Author(s):  
Stephen L. Young ◽  
Katherine Evans ◽  
Jerry P. Eu
Keyword(s):  
Nitric Oxide ◽  
Lung Development ◽  
Pulmonary Blood Flow ◽  
Cellular Proliferation ◽  
Branching Morphogenesis ◽  
Rat Lung ◽  
No Donors ◽  
Fetal Rat ◽  
Nos Inhibitors ◽  
Fetal Rat Lung

Cells of the developing lung express the constitutive nitric oxide synthases (NOSs) I and III. The developmental importance of these enzymes is largely unknown, although a role for nitric oxide (NO) in the regulation of pulmonary blood flow at birth is established. Known effects of NO on transcription factors, apoptosis, and cellular proliferation, plus the time and spatial limits of pulmonary NOS expression, suggest that NO might influence lung development. We tested the potential of NO to modulate lung branching morphogenesis by exposing lung explants from gestational day 13 rat fetuses to varying doses of several NO donors (NONO-ate). We counted the number of airway branches that were added between the first and 72nd h of culture. NO released only from a NONO-ate with a long half-life {( Z)-1-[2-(2-aminoethyl)- N-(2-ammonioethyl)amino]-diazen-1-ium-1,2-diolate-NO}, increased branching in ambient O2 by twofold. The NO effect was not mimicked with a cyclic guanine monophosphate analog; nonspecific NOS inhibitors in millimolar concentrations inhibited branching. We conclude that endogenous and exogenous NO can modulate branching morphogenesis in the rat lung.

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.

Late appearance of a type I alveolr epithelialar cell marker during fetal rat lung development

1994 ◽  
Vol 102 (4) ◽  
pp. 297-304 ◽  
Author(s):  
S. I. Danto ◽  
S. M. Zabski ◽  
E. D. Crandall
Keyword(s):  
Lung Development ◽  
Type I ◽  
Rat Lung ◽  
Cell Marker ◽  
Fetal Rat ◽  
Fetal Rat Lung

Expression of TGF-alpha, EGF, and EGF receptor in fetal rat lung

1994 ◽  
Vol 267 (4) ◽  
pp. L384-L389 ◽  
Author(s):  
T. P. Strandjord ◽  
J. G. Clark ◽  
D. K. Madtes
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Lung Development ◽  
Egf Receptor ◽  
Late Gestation ◽  
Rat Lung ◽  
Cultured Fibroblasts ◽  
Receptor Mrna ◽  
Fetal Rat ◽  
Fetal Rat Lung

To define the distribution of transforming growth factor-alpha (TGF-alpha) and its relationship to epidermal growth factor (EGF) and EGF receptor in lung development and to determine whether epithelial cells produce TGF-alpha, we studied the expression of TGF-alpha, EGF, and their receptor in late-gestation fetal rat lung and in cultured fetal rat lung cells. TGF-alpha, EGF, and EGF receptor were colocalized in epithelial and smooth muscle cells of bronchioles and bronchi and in epithelial cells of saccules. Epithelial cells cultured from late-gestation fetal rat lung transcribe TGF-alpha and EGF receptor mRNA and produce TGF-alpha and EGF receptor proteins. Cultured fibroblasts contained EGF receptor mRNA, but no detectable TGF-alpha mRNA. These results demonstrate fetal lung epithelial cells are a source for TGF-alpha and suggest that TGF-alpha might act through an autocrine or paracrine mechanism with epithelial and mesenchymal cells. The colocalization of TGF-alpha and EGF suggests that these growth factors might act in parallel in lung development.

Morphometric analysis of fetal rat lung after the administration of Pyralene-3000

1996 ◽  
Vol 431 (S6) ◽  
pp. R213-R214
Author(s):  
Milka Vrecl ◽  
Azra Pogačnik ◽  
J. Lorger ◽  
S. V. Bavdek
Keyword(s):  
Morphometric Analysis ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

scholarly journals The Role of Glycoprotein 130 Family of Cytokines in Fetal Rat Lung Development

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e67607 ◽  
Author(s):  
Cristina Nogueira-Silva ◽  
Paulina Piairo ◽  
Emanuel Carvalho-Dias ◽  
Carla Veiga ◽  
Rute S. Moura ◽  
...  
Keyword(s):  
Lung Development ◽  
Rat Lung ◽  
Fetal Rat ◽  
Fetal Rat Lung

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.

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