scholarly journals SUN-015 Glucocorticoid Induction And Direct Genomic Regulation Of The Transcriptional Regulators Hif3a And Zbtb16 During Fetal Mouse Lung Development

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Timothy Cole ◽  
Bennet Seow ◽  
Kelly Short
Keyword(s):  
Lung Development ◽  
Transcriptional Regulators ◽  
Mouse Lung ◽  
Fetal Mouse ◽  
Glucocorticoid Induction ◽  
Genomic Regulation

Laminin 2 attachment selects myofibroblasts from fetal mouse lung

1998 ◽  
Vol 275 (3) ◽  
pp. L622-L630
Author(s):  
Guillermo Flores-Delgado ◽  
Pablo Bringas ◽  
David Warburton
Keyword(s):  
Lung Development ◽  
Cell Biology ◽  
Smooth Muscle Actin ◽  
Primary Cultures ◽  
Fetal Lung ◽  
Mesenchymal Cells ◽  
Mouse Lung ◽  
Pcr Analysis ◽  
Rt Pcr ◽  
Fetal Mouse

Laminins (LNs) are extracellular matrix glycoproteins that are involved in cell adhesion, proliferation, and differentiation. So far, 11 LN variants (LN1 to LN11) have been described. In the lung, at least six LN variants have been identified. However, only the role of LN1 has been characterized to any extent. In this study, we hypothesized that the LN2 variant may play a role during lung development. We identified, by RT-PCR analysis, that the α2-chain mRNA of LN2 is expressed during mouse lung development. LN2 adhesion assays were then performed with cells from fetal mouse lung primary cultures. Our results showed that a specific subpopulation of fetal lung cells that expressed vimentin, α-smooth muscle actin, and desmin attached onto LN2, whereas the cells that did not adhere to LN2 as well as the total cell population were able to adhere readily on fibronectin. Cell attachment onto LN2 was inhibited by EDTA. In addition, we demonstrated, by RT-PCR and Western analysis, that the LN2-adherent cells autoexpressed the α2-chain of LN2. In the late pseudoglandular period, LN2 was localized by immunohistochemistry in the basement membrane of airways and blood vessels and around mesenchymal cells. We conclude that LN2 is expressed during lung development and that a specific subpopulation of fetal lung mesenchymal cells expressing a myofibroblastic phenotype can be selected by attachment to LN2 in primary culture. These findings lead us to speculate that LN2 may play a key role in the cell biology of myofibroblasts during lung development.

The Effect of Culture Conditions on Cytodifferentiation of Fetal Mouse Lung Respiratory Passageways

1986 ◽  
Vol 10 (2) ◽  
pp. 115-136 ◽  
Author(s):  
S. Robert Hilfer ◽  
Stephanie L. Schneck ◽  
Joyce W. Brown
Keyword(s):  
Culture Conditions ◽  
Mouse Lung ◽  
Fetal Mouse

Abrogation of mesenchyme-specific TGF-β signaling results in lung malformation with prenatal pulmonary cysts in mice

2021 ◽  
Author(s):  
Qing Miao ◽  
Hui Chen ◽  
Yongfeng Luo ◽  
Joanne Chiu ◽  
Ling Chu ◽  
...  
Keyword(s):  
Lung Development ◽  
Muscle Growth ◽  
Branching Morphogenesis ◽  
Mouse Lung ◽  
Cystic Lesions ◽  
Alveolar Epithelial ◽  
Pulmonary Cysts ◽  
Β Receptor ◽  
Airway Branching

The TGF-β signaling pathway plays a pivotal role in controlling organogenesis during fetal development. Although the role of TGF-β signaling in promoting lung alveolar epithelial growth has been determined, mesenchymal TGF-β signaling in regulating lung development has not been studied in vivo due to a lack of genetic tools for specifically manipulating gene expression in lung mesenchymal cells. Therefore, the integral roles of TGF-β signaling in regulating lung development and congenital lung diseases are not completely understood. Using a Tbx4 lung enhancer-driven Tet-On inducible Cre transgenic mouse system, we have developed a mouse model in which lung mesenchyme-specific deletion of TGF-β receptor 2 gene (Tgfbr2) is achieved. Reduced airway branching accompanied by defective airway smooth muscle growth and later peripheral cystic lesions occurred when lung mesenchymal Tgfbr2 was deleted from embryonic day 13.5 to 15.5, resulting in postnatal death due to respiratory insufficiency. Although cell proliferation in both lung epithelium and mesenchyme was reduced, epithelial differentiation was not significantly affected. Tgfbr2 downstream Smad-independent ERK1/2 may mediate these mesenchymal effects of TGF-β signaling through the GSK3β--β-catenin--Wnt canonical pathway in fetal mouse lung. Our study suggests that Tgfbr2-mediated TGF-β signaling in prenatal lung mesenchyme is essential for lung development and maturation, and defective TGF-β signaling in lung mesenchyme may be related to abnormal airway branching morphogenesis and congenital airway cystic lesions.

Differential expression of matrix metalloproteinases and their inhibitors in human and mouse lung development

2005 ◽  
Vol 94 (07) ◽  
pp. 175-183 ◽  
Author(s):  
Julie Ryu ◽  
Alfin G. Vicencio ◽  
Michael E. Yeager ◽  
Michael Kashgarian ◽  
Gabriel G. Haddad ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Development ◽  
Epithelial To Mesenchymal Transition ◽  
Developmental Stages ◽  
Human Lung ◽  
Matrix Metalloproteases ◽  
Mouse Lung ◽  
Mesenchymal Transition ◽  
Expression Arrays ◽  
Human And Mouse

SummaryLung development is a highly orchestrated process characterized by timed expression and activation of growth factor and protease/antiprotease systems. This interplay is essential in regulating vasculogenesis, alveolarization, and epithelial to mesenchymal transition during lung development. Alterations in the proteolytic/antiproteolytic balance of the lung have been associated with several respiratory diseases characterized by changes in the lung extracellular matrix (ECM). Here, we characterized the expression pattern of matrix metalloproteases (MMP) and their inhibitors, the tissue inhibitors of metalloproteases (TIMP), in human and mouse lung development. Using MMP/TIMP expression arrays, RT-PCR, Western Blotting, and ELISA analyses, we demonstrate that fetal human lung is characterized by a dominant proteolytic profile with high MMP-2 and little TIMP-3 expression. Adult human lung, in contrast, exhibits a more anti-proteolytic profile with decreased MMP-2 and increasedTIMP-3 expression. MMP-14, MMP-20,TIMP-1, and TIMP-2 were constitutively expressed, irrespective of the developmental stage. Similar results were obtained using mouse lungs of different developmental stages, with the addition that in mouse lung, TIMP-2 and TIMP-3 were upregulated as lung development progressed. Exposure of neonatal mice to chronic hypoxia (10% O2), a stimulus that leads to an arrest of lung development, resulted in upregulation of MMP-2 with a concomitant downregulation of TIMP-2.These results provide a comprehensive analysis of MMP and TIMP expression during human and mouse lung development. MMP-2, TIMP-2, and TIMP-3 may be key regulatory enzymes during lung development, possibly through their complex action on ECM components, membrane receptor ectodomain shedding, and growth factor bioactivity.

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