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FGF receptors control alveolar elastogenesis.

Rongbo Li1,2, John C Herriges2, Lin Chen3

  • 1Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.

Development (Cambridge, England)
|November 11, 2017
PubMed
Summary

Fibroblast Growth Factor (FGF) signaling via Fgfr3 and Fgfr4 receptors is vital for lung alveologenesis. This study reveals FGF signaling controls elastin production in lung mesenchyme, essential for forming gas-exchange surfaces.

Keywords:
AlveologenesisElastin extracellular matrixFGF signalingLung developmentMouse

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Area of Science:

  • Developmental Biology
  • Pulmonary Medicine
  • Genetics

Background:

  • Alveologenesis, the final stage of lung development, establishes the gas-exchange surface area but its genetic regulation is poorly understood.
  • Fibroblast Growth Factor (FGF) signaling through Fgfr3 and Fgfr4 receptors is known to be essential for alveologenesis, yet the precise mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the role of FGF signaling, specifically Fgfr3 and Fgfr4, in the genetic network governing alveologenesis.
  • To investigate the downstream mechanisms by which Fgfr3 and Fgfr4 mediate lung alveolar development.

Main Methods:

  • Utilized global Fgfr3;Fgfr4 double mutant mice to study lung development defects.
  • Performed mesenchymal and epithelial-specific gene inactivation to pinpoint the critical cell type.
  • Analyzed gene expression of elastogenesis machinery components and extracellular matrix (ECM) organization.

Main Results:

  • Fgfr3;Fgfr4 mutant mice exhibit alveolar simplification and elastin disorganization at the onset of alveologenesis.
  • Mesenchymal inactivation of Fgfr3 and Fgfr4, but not epithelial, recapitulated the observed lung defects.
  • Upregulation of MFAP5 (Myofibroblast Associated Protein 5), an elastin-microfibril bridging factor, was observed in mutants, and its mutation partially rescued the defects.

Conclusions:

  • FGF signaling, mediated by Fgfr3 and Fgfr4 in the lung mesenchyme, restricts the expression of elastogenic machinery during lung maturation.
  • This regulation ensures orderly formation of the elastin extracellular matrix, which is critical for driving alveolar septa formation and increasing the gas-exchange surface area.