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Front. Genet. | doi: 10.3389/fgene.2018.00418

Fgf10 Signaling in Lung Development, Homeostasis, Disease and Repair After Injury

 Tingting Yuan1,  Thomas Volckaert1, Diptiman Chanda1, Victor J. Thannickal1 and  Stijn P. De Langhe1*
  • 1University of Alabama at Birmingham, United States

The lung is morphologically structured into a complex tree-like network with branched airways ending distally in a large number of alveoli for efficient oxygen exchange. At the cellular level, the adult lung consists of at least 40-60 different cell types which can be broadly classified into epithelial, endothelial, mesenchymal, and immune cells. Fibroblast growth factor 10 (Fgf10) located in the lung mesenchyme is essential to regulate epithelial proliferation and lineage commitment during embryonic development and postnatal life, and to drive epithelial regeneration after injury. The cells that express Fgf10 in the mesenchyme are progenitors for mesenchymal cell lineages during embryonic development. During adult lung homeostasis, Fgf10 is expressed in mesenchymal stromal niches, between cartilage rings in the upper conducting airways where basal cells normally reside, and in the lipofibroblasts adjacent to alveolar type 2 cells. Fgf10 protects and promotes lung epithelial regeneration after different types of lung injuries. An Fgf10-Hippo epithelial-mesenchymal crosstalk ensures maintenance of stemness and quiescence during homeostasis and basal stem cell (BSC) recruitment to further promote regeneration in response to injury. Fgf10 signaling is dysregulated in different human lung diseases including bronchopulmonary dysplasia (BPD), idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD), suggesting that dysregulation of the FGF10 pathway is critical to the pathogenesis of several human lung diseases.

Keywords: Fgf10, Regeneration, Lung, Fibrosis, injury

Received: 06 Aug 2018; Accepted: 06 Sep 2018.

Edited by:

Saverio Bellusci, Justus Liebig Universität Gießen, Germany

Reviewed by:

Konstantinos Gkatzis, Max-Planck-Institut für Herz- und Lungenforschung, Germany
Emma Rawlins, University of Cambridge, United Kingdom  

Copyright: © 2018 Yuan, Volckaert, Chanda, Thannickal and De Langhe. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Stijn P. De Langhe, University of Alabama at Birmingham, Birmingham, 35294, Alabama, United States, sdelanghe@uabmc.edu