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Foxc2 influences alveolar epithelial cell differentiation during lung development

Journal article
Authors M. Tsuji
M. Morishima
K. Shimizu
S. Morikawa
Mikael Heglind
Sven Enerbäck
T. Ezaki
J. Tamaoki
Published in Development Growth & Differentiation
Volume 59
Issue 6
Pages 501-514
ISSN 0012-1592
Publication year 2017
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 501-514
Language en
Links dx.doi.org/10.1111/dgd.12368
Keywords alveolar progenitor cell, Foxc2, Lef1, lung development, mouse, lymphedema-distichiasis syndrome, keratinocyte growth-factor, griffonia, simplicifolia-i, beta-catenin, transcription factor, branching, morphogenesis, lycopersicon-esculentum, development suggests, endothelial-cells, fgf10 expression, Cell Biology
Subject categories Medical cell biology

Abstract

FOXC2, a forkhead transcriptional factor, is a candidate gene for congenital heart diseases and lymphedema-distichiasis syndrome and yellow nail syndrome; however, there are no reports on Foxc2 and the development of the lung. We have identified lung abnormalities in Foxc2-knockout embryos during investigation of cardiac development. The aim of this study was to clarify the morphological characteristics during lung development using ICR-Foxc2 knockout lungs. Mutant fetuses at embryonic days 10.5-18.5 were obtained from mating of Foxc2(+/-) mice and then analyzed. Notably, Foxc2-knockout lungs appeared parenchymatous and much smaller than those of the wild-type littermates. In the Foxc2 knockout lungs, the capillary beds remained distant from the alveolar epithelium until the late stages, the number of type2 alveolar cells per alveolar progenitor cell was lower and the type1 alveolar cells were thicker in Foxc2 knockout mice. In contrast, Foxc2 expression was only detected in the mesenchyme of the lung buds at E10.5, and it disappeared at E11.5 in Foxc2-LacZ knockin mice. Furthermore, the expression of Lef1 was significantly inhibited in E11.5 lungs. All of these results suggest that the abnormalities in Foxc2 knockout mice may involve maldifferentiation of alveolar epithelial cells and capillary vessel endothelial-alveolar epithelial approach as well as lymph vessel malformation. This is the first report about relationship between Foxc2 and lung development. This animal model might provide an important clue for elucidating the mechanism of lung development and the cause of respiratory diseases.

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