The structure of the respiratory portion of the mammalian lung with notes on the lining of the frog lung

1938 ◽  
Vol 62 (3) ◽  
pp. 375-425 ◽  
Author(s):  
Clayton G. Loosli
Keyword(s):  
Mammalian Lung

scholarly journals Development and Remodeling of the Vertebrate Blood-Gas Barrier

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Andrew Makanya ◽  
Aikaterini Anagnostopoulou ◽  
Valentin Djonov
Keyword(s):  
Extracellular Proteins ◽  
Appreciable Amount ◽  
Interstitial Tissue ◽  
Type I ◽  
Blood Gas ◽  
Gas Barrier ◽  
Molecular Control ◽  
Blood Capillaries ◽  
Mammalian Lung ◽  
Avian Lung

During vertebrate development, the lung inaugurates as an endodermal bud from the primitive foregut. Dichotomous subdivision of the bud results in arborizing airways that form the prospective gas exchanging chambers, where a thin blood-gas barrier (BGB) is established. In the mammalian lung, this proceeds through conversion of type II cells to type I cells, thinning, and elongation of the cells as well as extrusion of the lamellar bodies. Subsequent diminution of interstitial tissue and apposition of capillaries to the alveolar epithelium establish a thin BGB. In the noncompliant avian lung, attenuation proceeds through cell-cutting processes that result in remarkable thinning of the epithelial layer. A host of morphoregulatory molecules, including transcription factors such as Nkx2.1, GATA, HNF-3, and WNT5a; signaling molecules including FGF, BMP-4, Shh, and TFG-βand extracellular proteins and their receptors have been implicated. During normal physiological function, the BGB may be remodeled in response to alterations in transmural pressures in both blood capillaries and airspaces. Such changes are mitigated through rapid expression of the relevant genes for extracellular matrix proteins and growth factors. While an appreciable amount of information regarding molecular control has been documented in the mammalian lung, very little is available on the avian lung.

scholarly journals Spry2 regulates signalling dynamics and terminal bud branching behaviour during lung development

2015 ◽  
Vol 97 ◽  
Author(s):  
YINGYING ZHAO ◽  
TIMOTHY P. O'BRIEN
Keyword(s):  
Lung Development ◽  
Development Stage ◽  
Cystic Structure ◽  
Signalling Network ◽  
Terminal Bud ◽  
Elevated Expression ◽  
Mammalian Lung ◽  
Fgf Signalling ◽  
Cellular Responsiveness ◽  
Bac Transgene

SummaryDevelopment of mammalian lung involves reiterative outgrowth and branching of an epithelial tube into the surrounding mesenchymal bed. Each coordinated growth and branching cycle is driven by reciprocal signalling between epithelial and adjacent mesenchymal cells. This signalling network includes FGF, SHH, BMP4 and other pathways. We have characterized lung defects in 36Pub mice carrying a deletion that removes an antagonist of FGF signalling, Spry2. Spry2 deficient mice show an enlarged cystic structure located in the terminus of each lobes. Our study shows that Spry2 deficient lungs have reduced lung branching and the cystic structure forms in the early lung development stage. Furthermore, mice carrying a targeted disruption of Spry2 fail to complement the lung phenotype characterized in 36Pub mice. A Spry2-BAC transgene rescues the defect. Interestingly, cystic structure growth is accompanied by the reduced and spatially disorganized expression of Fgf10 and elevated expression of Shh and Bmp4. Altered signalling balance due to the loss of Spry2 causes a delayed branch cycle and cystic growth. Our data underscores the importance of restricting cellular responsiveness to signalling and highlights the interplay between morphogenesis events and spatial localization of gene expression.

Sign in / Sign up

Export Citation Format

Share Document