CM Chao

D Alam

H Ehrhardt

KP Zimmer

S Bellusci

S Schermuly

Molecular and Cellular Pediatrics

PubMed

Springer - Publisher Connector

Impact of embryonic Fgf10 expression deficiency on embryonic 
mouse lung development and repair following hyperoxia injury 
 
CM Chao,
Aff1 Aff3 
Corresponding Affiliation: Aff1 
 
D Al Alam,
Aff2 
 
S Schermuly,
Aff3 
 
H Ehrhardt,
Aff1 
 
KP Zimmer,
Aff1 
 
S Bellusci,
Aff3 
 
ArticleInfo 
ArticleID : 54 
ArticleDOI : 10.1186/2194-7791-2-S1-A14 
ArticleCitationID : A14 
ArticleSequenceNumber : 14 
ArticleCategory : Meeting abstract 
ArticleFirstPage : 1 
ArticleLastPage : 2 
ArticleHistory : 
RegistrationDate : 2015–7–1 
OnlineDate : 2015–7–1 
 
ArticleCopyright : 
Chao et al.2015 
This article is published under license to BioMed Central 
Ltd. This is an Open Access article distributed under the 
terms of the Creative Commons Attribution License 
(http://creativecommons.org/licenses/by/4.0), which permits 
unrestricted use, distribution, and reproduction in any 
medium, provided the original work is properly cited. 
 
Aff1 
Justus-Liebig-Universität,  Gießen,  Germany 
 
Aff2 
Saban Research Institute,  Los Angeles,  CA,  USA 
 
Aff3 
Excellence Cluster Cardio-Pulmonary System,  Gießen,  Germany 
 
 
Abstracts of the 51st Workshop for Pediatric Research 
 51st Workshop for Pediatric Research 
 
Göttingen, Germany 
 
16-17 April 2015 
 
This supplement has not been sponsored. 
 
Meeting abstracts 
 
Background 
Bronchopulmonary dysplasia (BPD), a chronic lung disease of preterm infants, is characterized by impaired 
alveolar growth and pathologic vascularization. 
Aims 
To investigate the impact of Fgf10 expression deficiency on embryonic lung development and hyperoxia lung 
injury (BPD mouse model). 
Methods 
1) Embryonic lungs (Fgf10
+/-
 and Fgf10
+/+
[WT]) were harvested at E12.5 and E18.5. Lung branches were 
quantified and H&E staining was performed. 
2) After BrdU labeling lungs were harvest from embryos at E12.5. BrdU staining was performed on 
paraffin-embedded sections. 
3) Transcriptomic analyses were performed by using whole lung RNA isolated at E18.5. 
4) BPD mouse model: 
Fgf10
+/-
 and Fgf10
+/+
 mice were exposed to 85% O2 from P0-P8. Lung morphometric analysis, IHC staining 
(α-Actin/vWF staining, SPC, E-cadherin, Ki67, TUNEL), gene expression analysis (RNA isolated from type II 
alveolar epithelial cells [AEC II]), FACS (epithelial/ mesenchymal progenitor cells, AEC I/ II) were performed at 
P3. 
Results 
1) Embryonic Fgf10 heterozygous lungs exhibit epithelial branching defects and decreased Fibroblast growth 
factor signaling. 
2) Embryonic Fgf10
+/-
 lungs show decreased epithelial proliferation. 
3) Lungs of E18.5 Fgf10
+/-
 embryos display structural defects and abnormal gene expression. 
4) Fgf10 heterozygous pups display increased sensitivity to hyperoxia exposure associated with significant 
structural lung defects. Transcriptomic analyses show epithelial defects linked to cell cycle dysregulation 
and increased Tgfb signaling. Fgf10 heterozygous vessels are more sensitive to hyperoxia injury and 
exhibit a less muscularized phenotype. SPC staining shows significant decrease in SPC+ cells after 
hyperoxia injury. FACS analysis revealed an increase of AEC I on the expenses of AEC II (progenitor 
cell). 
Conclusion 
Fgf10 deficiency leads to impaired embryonic lung development and death upon postnatal hyperoxia lung injury 
due to vulnerability of the epithelium. 


Impact of embryonic Fgf10 expression deficiency on embryonic mouse lung development and repair following hyperoxia injury

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https://molcellped.springeropen.com/track/pdf/10.1186/2194-7791-2-S1-A14?site=molcellped.springeropen.com

Impact of embryonic Fgf10 expression deficiency on embryonic mouse lung development and repair following hyperoxia injury

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