Maturational Factors Modulate Transcription Factors CCAAT/Enhancer-Binding Proteins α, β, δ, and Peroxisome Proliferator–Activated Receptor-γ in Fetal Rat Lung Epithelial Cells

2003 ◽  
Vol 29 (5) ◽  
pp. 620-626 ◽  
Author(s):  
Anne-Marie Barlier-Mur ◽  
Bernadette Chailley-Heu ◽  
Claudie Pinteur ◽  
Alexandra Henrion-Caude ◽  
Christophe Delacourt ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Epithelial Cells ◽  
Binding Proteins ◽  
Lung Epithelial Cells ◽  
Peroxisome Proliferator ◽  
Rat Lung ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Fetal Rat Lung

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

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 Activation of the mTORC1/PGC-1 axis promotes mitochondrial biogenesis and induces cellular senescence in the lung epithelium

2019 ◽  
Vol 316 (6) ◽  
pp. L1049-L1060 ◽  
Author(s):  
Ross Summer ◽  
Hoora Shaghaghi ◽  
DeLeila Schriner ◽  
Willy Roque ◽  
Dominic Sales ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cellular Senescence ◽  
Mitochondrial Biogenesis ◽  
Lung Epithelial Cells ◽  
Chronic Obstructive ◽  
Protective Mechanism ◽  
Peroxisome Proliferator ◽  
Lung Epithelium ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lung Epithelial

Cellular senescence is a biological process by which cells lose their capacity to proliferate yet remain metabolically active. Although originally considered a protective mechanism to limit the formation of cancer, it is now appreciated that cellular senescence also contributes to the development of disease, including common respiratory ailments such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. While many factors have been linked to the development of cellular senescence, mitochondrial dysfunction has emerged as an important causative factor. In this study, we uncovered that the mitochondrial biogenesis pathway driven by the mammalian target of rapamycin/peroxisome proliferator-activated receptor-γ complex 1α/β (mTOR/PGC-1α/β) axis is markedly upregulated in senescent lung epithelial cells. Using two different models, we show that activation of this pathway is associated with other features characteristic of enhanced mitochondrial biogenesis, including elevated number of mitochondrion per cell, increased oxidative phosphorylation, and augmented mitochondrial reactive oxygen species (ROS) production. Furthermore, we found that pharmacological inhibition of the mTORC1 complex with rapamycin not only restored mitochondrial homeostasis but also reduced cellular senescence to bleomycin in lung epithelial cells. Likewise, mitochondrial-specific antioxidant therapy also effectively inhibited mTORC1 activation in these cells while concomitantly reducing mitochondrial biogenesis and cellular senescence. In summary, this study provides a mechanistic link between mitochondrial biogenesis and cellular senescence in lung epithelium and suggests that strategies aimed at blocking the mTORC1/PGC-1α/β axis or reducing ROS-induced molecular damage could be effective in the treatment of senescence-associated lung diseases.

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