Dataset Information

FGF Signaling in Lung Development and Disease: Human Versus Mouse.

ABSTRACT: Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is no evidence of a causative role for FGF10 or these SNPs in human lung development and pediatric lung diseases. We and others have shown divergent roles for FGF10 in mouse lung development and early human lung development. Herein, we only review the existing literature on FGF signaling in human lung development and pediatric human lung diseases, comparing what is known in mouse lung to that in human lung.

SUBMITTER: Danopoulos S

PROVIDER: S-EPMC6423913 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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FGF Signaling in Lung Development and Disease: Human Versus Mouse.

Danopoulos Soula S Shiosaki Jessica J Al Alam Denise D

Frontiers in genetics 20190312

Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is no evidence of a causative role for FGF10 or these SNPs in human lung development and pediatric lung diseases. We and others have shown divergent roles for FGF10 in mouse lung development and early hu ...[more]

PMID: 30930931

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Project description:Fibroblast growth factor (FGF) signaling plays an important role in lung organogenesis. Over recent decades, FGF signaling in lung development has been extensively studied in animal models. However, little is known about the expression, localization, and functional roles of FGF ligands during human fetal lung development. Therefore, we aimed to determine the expression and function of several FGF ligands and receptors in human lung development. Using in situ hybridization (ISH) and RNA sequencing, we assessed their expression and distribution in native human fetal lung. Human fetal lung explants were treated with recombinant FGF7, FGF9, or FGF10 in air-liquid interface culture. Explants were analyzed grossly to observe differences in branching pattern as well as at the cellular and molecular level. ISH demonstrated that FGF7 is expressed in both the epithelium and mesenchyme; FGF9 is mainly localized in the distal epithelium, whereas FGF10 demonstrated diffuse expression throughout the parenchyma, with some expression in the smooth muscle cells (SMCs). FGFR2 expression was high in both proximal and distal epithelial cells as well as the SMCs. FGFR3 was expressed mostly in the epithelial cells, with lower expression in the mesenchyme, while FGFR4 was highly expressed throughout the mesenchyme and in the distal epithelium. Using recombinant FGFs, we demonstrated that FGF7 and FGF9 had similar effects on human fetal lung as on mouse fetal lung; however, FGF10 caused the human explants to expand and form cysts as opposed to inducing epithelial branching as seen in the mouse. In conjunction with decreased branching, treatment with recombinant FGF7, FGF9, and FGF10 also resulted in decreased double-positive SOX2/SOX9 progenitor cells, which are exclusively present in the distal epithelial tips in early human fetal lung. Although FGF ligand localization may be somewhat comparable between developing mouse and human lungs, their functional roles may differ substantially. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Dataset Information

FGF Signaling in Lung Development and Disease: Human Versus Mouse.

Publications

FGF Signaling in Lung Development and Disease: Human Versus Mouse.

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