Efficient regulation of branching morphogenesis via fibroblast growth factor receptor 2c in early-stage embryonic mouse salivary glands

2016 ◽  
Vol 92 (4) ◽  
pp. 216-224
Author(s):  
Minami Shibuya ◽  
Tatsuya Ikari ◽  
Goro Sugiyama ◽  
Yukiko Ohyama ◽  
Wataru Kumamaru ◽  
...  
Keyword(s):  
Growth Factor ◽  
Salivary Glands ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Early Stage ◽  
Growth Factor Receptor ◽  
Branching Morphogenesis ◽  
Fibroblast Growth ◽  
Embryonic Mouse

scholarly journals 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

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1274
Author(s):  
Matthew R. Jones ◽  
Arun Lingampally ◽  
Jin Wu ◽  
Jamschid Sedighi ◽  
Negah Ahmadvand ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Lung Development ◽  
Fibroblast Growth Factor Receptor ◽  
Biological Activities ◽  
Growth Factor Receptor ◽  
Branching Morphogenesis ◽  
Soluble Form ◽  
Alveolar Type ◽  
Fibroblast Growth

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.

Characterization of Fibroblast Growth Factor Receptor 1 RNA Expression in the Embryonic Mouse Heart

1995 ◽  
Vol 752 (1 Cardiac Growt) ◽  
pp. 406-416 ◽  
Author(s):  
KISHORE B. S. PASUMARTHI ◽  
YAN JIN ◽  
MARGARET E. BOCK ◽  
ARISTIDES LYTRAS ◽  
ELISSAVET KARDAMI ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Mouse Heart ◽  
Rna Expression ◽  
Fibroblast Growth ◽  
Embryonic Mouse

scholarly journals Deletion of Frs2α from the ureteric epithelium causes renal hypoplasia

2009 ◽  
Vol 297 (5) ◽  
pp. F1208-F1219 ◽  
Author(s):  
Sunder Sims-Lucas ◽  
Luise Cullen-McEwen ◽  
Veraragavan P. Eswarakumar ◽  
David Hains ◽  
Kayle Kish ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Point Mutations ◽  
Growth Factor Receptor ◽  
Branching Morphogenesis ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
Renal Hypoplasia ◽  
Branching Architecture

Fibroblast growth factor receptor 2 (Fgfr2) signaling is critical in maintaining ureteric branching architecture and mesenchymal stromal morphogenesis in the kidney. Fibroblast growth factor receptor substrate 2α (Frs2α) is a major docking protein for Fgfr2 with downstream targets including Ets variant (Etv) 4 and Etv5 in other systems. Furthermore, global deletion of Frs2α causes early embryonic lethality. The purpose of the study was to determine the role of Frs2α in mediating Fgfr2 signaling in the ureteric epithelium. To that end, we generated mice with conditional deletion of Frs2α in the ureteric epithelium ( Frs2α UB−/−) and mice with point mutations in the Frs2α binding site of Fgfr2 ( Fgfr2 LR/LR). Frs2α UB−/− mice developed mild renal hypoplasia characterized by decreased ureteric branching morphogenesis but maintained normal overall branching architecture and had normal mesenchymal stromal development. Reduced nephron endowment in postnatal mutant mice was observed, corresponding with the reduction in branching morphogenesis. Furthermore, there were no apparent renal abnormalities in Fgfr2 LR/LR mice. Interestingly, Etv4 and Etv5 expression was unaltered in Frs2α UB−/− mice, as was Sprouty1, an antagonist of Frs2α signaling. However, Ret and Wnt11 (molecules critical for ureteric branching morphogenesis) mRNA levels were lower in mutants vs. controls. Taken together, these findings suggest that Fgfr2 signals through adapter molecules other than Frs2α in the ureteric epithelium. Furthermore, Frs2α may transmit signals through other receptor kinases present in ureteric epithelium. Finally, the renal hypoplasia observed in Frs2α UB−/− mice is likely secondary to decreased Ret and Wnt11 expression.

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