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Cells
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FGF Signaling in Lung Development, Homeostasis and Disease
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FGF Signaling in Lung Development, Homeostasis and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 10967

Special Issue Editor

Prof. Dr. Saverio Bellusci

E-Mail Website
Guest Editor
Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, member of the German Center for Lung Research, Justus-Liebig-University Giessen, 35392 Giessen, Germany
Interests: lung development and regeneration/repair; fibroblast growth factors; epithelial stem cells; resident stromal niche; lipofibroblasts; fibrosis

Special Issue Information

Dear Colleagues,

The fibroblast growth factor (FGF) family comprises secreted growth factors acting via tyrosine kinase receptors (FGFRs). FGF signaling occurs both in the epithelium and mesenchyme and thereby orchestrates epithelial–mesenchymal interactions taking place during the different stages of lung development and homeostasis. FGF signaling has been shown to be critical for the formation of multiple epithelial and mesenchymal lineages in the lung and is also re-engaged during the repair process following injury. Such signaling can also be impaired or abnormally activated in pathological processes such as cancer or fibrosis. In this Special Issue, we also aim to analyze the impact of FGF signaling on stem cells in the context of lung regeneration. In particular, contributions involving single cell transcriptomic, genetic manipulation of genes in specific lineages are encouraged. Both original research articles and reviews will be considered.

Prof. Saverio Bellusci
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • FGF
  • FGFR
  • FGF signaling
  • stem cells
  • epithelial and mesenchymal lineages
  • repair
  • fibrosis
  • emphysema
  • cancer

Published Papers (3 papers)

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Research

19 pages, 2808 KiB  
Article
Fibroblast Growth Factor—14 Acts as Tumor Suppressor in Lung Adenocarcinomas
by Kati Turkowski, Frederik Herzberg, Stefan Günther, David Brunn, Andreas Weigert, Michael Meister, Thomas Muley, Mark Kriegsmann, Marc A. Schneider, Hauke Winter, Michael Thomas, Friedrich Grimminger, Werner Seeger, Soni Savai Pullamsetti and Rajkumar Savai
Cells 2020, 9(8), 1755; https://doi.org/10.3390/cells9081755 - 22 Jul 2020
Cited by 10 | Viewed by 4785
Abstract
Investigation of the molecular dynamics in lung cancer is crucial for the development of new treatment strategies. Fibroblast growth factor (FGF) 14 belongs to the FGF family, which might play a crucial role in cancer progression. We analyzed lung adenocarcinoma (LUAC) patients samples [...] Read more.
Investigation of the molecular dynamics in lung cancer is crucial for the development of new treatment strategies. Fibroblast growth factor (FGF) 14 belongs to the FGF family, which might play a crucial role in cancer progression. We analyzed lung adenocarcinoma (LUAC) patients samples and found that FGF14 was downregulated, correlating with reduced survival and oncogenic mutation status. FGF14 overexpression in lung cancer cell lines resulted in decreased proliferation, colony formation, and migration, as well as increased expression of epithelial markers and a decreased expression of mesenchymal markers, indicating a mesenchymal to epithelial transition in vitro. We verified these findings using small interfering RNA against FGF14 and further confirmed the suppressive effect of FGF14 in a NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ immunodeficient xenograft tumor model. Moreover, FGF14 overexpressing tumor cell RNA sequencing data suggests that genes affected by FGF14 were related to the extracellular matrix, playing a role in proliferation and migration. Notably, newly identified FGF14 target genes, adenosine deaminase RNA specific B1 (ADARB1), collagen and calcium-binding epidermal growth factor domain-containing protein 1 (CCBE1), α1 chain of collagen XI (COL11A1), and mucin 16 (MUC16) expression was negatively correlated with overall survival when FGF14 was downregulated in LUAC. These findings led us to suggest that FGF14 regulates proliferation and migration in LUAC. Full article
(This article belongs to the Special Issue FGF Signaling in Lung Development, Homeostasis and Disease)
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19 pages, 10898 KiB  
Article
Evidence for Overlapping and Distinct Biological Activities and Transcriptional Targets Triggered by Fibroblast Growth Factor Receptor 2b Signaling between Mid- and Early Pseudoglandular Stages of Mouse Lung Development
by Matthew R. Jones, Arun Lingampally, Jin Wu, Jamschid Sedighi, Negah Ahmadvand, Jochen Wilhelm, Ana Ivonne Vazquez-Armendariz, Susanne Herold, Chengshui Chen, Jin-San Zhang, Saverio Bellusci and Cho-Ming Chao
Cells 2020, 9(5), 1274; https://doi.org/10.3390/cells9051274 - 21 May 2020
Cited by 11 | Viewed by 2691
Abstract
Branching morphogenesis is the basic developmental mode common to organs such as the lungs that undergo a process of ramification from a rudimentary tree. However, the precise molecular and cellular bases underlying the formation of branching organs are still unclear. As inactivation of [...] Read more.
Branching morphogenesis is the basic developmental mode common to organs such as the lungs that undergo a process of ramification from a rudimentary tree. However, the precise molecular and cellular bases underlying the formation of branching organs are still unclear. As inactivation of fibroblast growth factor receptor 2b (Fgfr2b) signaling during early development leads to lung agenesis, thereby preventing the analysis of this pathway at later developmental stages, we used transgenic mice to induce expression of a soluble form of Fgfr2b to inactivate Fgfr2b ligands at embryonic day (E) 14.5, corresponding to the mid-pseudoglandular stage of lung development. We identified an Fgfr2b signaling signature comprised of 46 genes enriched in the epithelium, some of which were common to, but most of them distinct from, the previously identified Fgfr2b signaling signature at E12.5. Our results indicate that Fgfr2b signaling at E14.5 controls mostly proliferation and alveolar type 2 cell (AT2) differentiation. In addition, inhibition of Fgfr2b signaling at E14.5 leads to morphological and cellular impairment at E18.5, with defective alveolar lineage formation. Further studies will have to be conducted to elucidate the role of Fgfr2b signaling at successive stages (canalicular/saccular/alveolar) of lung development as well as during homeostasis and regeneration and repair after injury. Full article
(This article belongs to the Special Issue FGF Signaling in Lung Development, Homeostasis and Disease)
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Figure 1

21 pages, 6582 KiB  
Article
Failure to Down-Regulate miR-154 Expression in Early Postnatal Mouse Lung Epithelium Suppresses Alveologenesis, with Changes in Tgf-β Signaling Similar to those Induced by Exposure to Hyperoxia
by Cho-Ming Chao, Gianni Carraro, Zvonimir A. Rako, Johannes Kolck, Jamschid Sedighi, Volker Zimmermann, Alena Moiseenko, Jochen Wilhelm, Brittany M. Young, Lei Chong, Jin Wu, Adriana Contreras, Parviz Minoo, Guillermo Barreto, David Warburton and Saverio Bellusci
Cells 2020, 9(4), 859; https://doi.org/10.3390/cells9040859 - 02 Apr 2020
Cited by 6 | Viewed by 3011
Abstract
Background: Bronchopulmonary dysplasia (BPD) is a lung disease of preterm born infants, characterized by alveolar simplification. MicroRNA (miR) are known to be involved in many biological and pathological processes in the lung. Although a changed expression has been described for several miR [...] Read more.
Background: Bronchopulmonary dysplasia (BPD) is a lung disease of preterm born infants, characterized by alveolar simplification. MicroRNA (miR) are known to be involved in many biological and pathological processes in the lung. Although a changed expression has been described for several miR in BPD, a causal role remains to be established. Results: Our results showed that the expression level of miR-154 increases during lung development and decreases postnatally. Further, hyperoxia treatment maintains high levels of miR-154 in alveolar type 2 cells (AT2). We hypothesized that the decrease in miR-154 expression in AT2 cells is required for normal alveologenesis. To test this hypothesis, we generated a novel transgenic mouse allowing doxycycline-based miR-154 overexpression. Maintenance of miR-154 expression in the postnatal distal lung epithelium under normoxia conditions is sufficient to reproduce the hypoalveologenesis phenotype triggered by hyperoxia. Using a pull-down assay, we identified Caveolin1 as a key downstream target of miR-154. Caveolin1 protein is downregulated in response to overexpression of miR-154. This is associated with increased phosphorylation of Smad3 and Tgf-ß signaling. We found that AT2 cells overexpressing miR-154 display decreased expression of AT2 markers and increased expression of AT1 markers. Conclusion: Our results suggest that down-regulation of miR-154 in postnatal lung may function as an important physiological switch that permits the induction of the correct alveolar developmental program, while conversely, failure to down-regulate miR-154 suppresses alveolarization, leading to the common clinically observed phenotype of alveolar simplification. Full article
(This article belongs to the Special Issue FGF Signaling in Lung Development, Homeostasis and Disease)
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