scholarly journals Simulations demonstrate a simple network to be sufficient to control branch point selection, smooth muscle and vasculature formation during lung branching morphogenesis

Biology Open ◽  
2012 ◽  
Vol 1 (8) ◽  
pp. 775-788 ◽  
Author(s):  
G. Celliere ◽  
D. Menshykau ◽  
D. Iber
Keyword(s):  
Smooth Muscle ◽  
Branch Point ◽  
Branching Morphogenesis ◽  
Point Selection ◽  
Simple Network ◽  
Lung Branching ◽  
Control Branch

Smad1 expression and function during mouse embryonic lung branching morphogenesis

2005 ◽  
Vol 288 (6) ◽  
pp. L1033-L1039 ◽  
Author(s):  
Cheng Chen ◽  
Hui Chen ◽  
Jianping Sun ◽  
Pablo Bringas ◽  
Yuhua Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Expression Patterns ◽  
Branching Morphogenesis ◽  
Mesenchymal Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Embryonic Lung ◽  
Embryonic Mouse ◽  
Lung Branching

Bone morphogenetic protein (BMP) 4 plays very important roles in regulating developmental processes of many organs, including lung. Smad1 is one of the BMP receptor downstream signaling proteins that transduce BMP4 ligand signaling from cell surface to nucleus. The dynamic expression patterns of Smad1 in embryonic mouse lungs were examined using immunohistochemistry. Smad1 protein was predominantly detected in peripheral airway epithelial cells of early embryonic lung tissue [embryonic day 12.5 (E12.5)], whereas Smad1 protein expression in mesenchymal cells increased during mid-late gestation. Many Smad1-positive mesenchymal cells were localized adjacent to large airway epithelial cells and endothelial cells of blood vessels, which colocalized with a molecular marker of smooth muscle cells (α-smooth muscle actin). The biological function of Smad1 in early lung branching morphogenesis was then studied in our established E11.5 lung explant culture model. Reduction of endogenous Smad1 expression was achieved by adding a Smad1-specific antisense DNA oligonucleotide, causing ∼20% reduction of lung epithelial branching. Furthermore, airway epithelial cell proliferation and differentiation were also inhibited when endogenous Smad1 expression was knocked down. Therefore, these data indicate that Smad1, acting as an intracellular BMP signaling pathway component, positively regulates early mouse embryonic lung branching morphogenesis.

scholarly journals Abrogation of Transforming Growth Factor-β Type II Receptor Stimulates Embryonic Mouse Lung Branching Morphogenesis in Culture

1996 ◽  
Vol 180 (1) ◽  
pp. 242-257 ◽  
Author(s):  
Jingsong Zhao ◽  
Ding Bu ◽  
Matt Lee ◽  
Harold C. Slavkin ◽  
Frederick L. Hall ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Branching Morphogenesis ◽  
Mouse Lung ◽  
Type Ii ◽  
Embryonic Mouse ◽  
Lung Branching

scholarly journals Impaired Lung Branching Morphogenesis in the Absence of Functional EGF Receptor

1997 ◽  
Vol 186 (2) ◽  
pp. 224-236 ◽  
Author(s):  
Päivi J. Miettinen ◽  
David Warburton ◽  
Ding Bu ◽  
Jing-Song Zhao ◽  
Joel E. Berger ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Branching Morphogenesis ◽  
Lung Branching

scholarly journals Models of lung branching morphogenesis

2015 ◽  
Vol 157 (3) ◽  
pp. 121-127 ◽  
Author(s):  
T. Miura
Keyword(s):  
Branching Morphogenesis ◽  
Lung Branching

scholarly journals Localized Fgf10 expression is not required for lung branching morphogenesis but prevents differentiation of epithelial progenitors

Development ◽  
2013 ◽  
Vol 140 (18) ◽  
pp. 3731-3742 ◽  
Author(s):  
T. Volckaert ◽  
A. Campbell ◽  
E. Dill ◽  
C. Li ◽  
P. Minoo ◽  
...  
Keyword(s):  
Branching Morphogenesis ◽  
Fgf10 Expression ◽  
Lung Branching

PDGF-AA and its receptor influence early lung branching via an epithelial-mesenchymal interaction

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2559-2567 ◽  
Author(s):  
P. Souza ◽  
M. Kuliszewski ◽  
J. Wang ◽  
I. Tseu ◽  
A.K. Tanswell ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Critical Role ◽  
Polymerase Chain Reaction Analysis ◽  
Branching Morphogenesis ◽  
Inhibitory Effect ◽  
Embryonic Lung ◽  
Morphometric Analyses ◽  
Terminal Buds ◽  
Lung Branching

The biological role of platelet-derived growth factor (PDGF)-AA in lung morphogenesis was investigated by incubating embryonic lung explants with phosphorothioate antisense PDGF-A oligonucleotides, which decreased PDGF-AA but not PDGF-BB protein content. Antisense PDGF-A oligonucleotides inhibited DNA synthesis. This inhibitory effect of antisense PDGF-A was reversed by the addition of exogenous PDGF-AA but not PDGF-BB. Morphometric analyses of antisense-treated cultures showed a significant reduction in lung size. The number of terminal buds of the lung explants was significantly decreased by antisense PDGF-A oligonucleotides. PDGF-AA but not PDGF-BB attenuated the inhibitory effect of antisense PDGF-A on early lung branching. Sense PDGF-A had no effect on DNA synthesis and early lung branching. Reverse transcriptase-polymerase chain reaction analysis revealed PDGF-A mRNA expression in the epithelial component of the embryonic lung, while message for PDGF alpha-receptor was expressed in the mesenchyme. Incubation of explants with neutralizing PDGF-AA antibodies also reduced DNA synthesis and early branching morphogenesis. We conclude that PDGF-AA and its receptor represent an important epithelial-mesenchymal interaction which plays a critical role in early lung branching morphogenesis.

Sign in / Sign up

Export Citation Format

Share Document