FGF receptors 1 and 2 are key regulators of keratinocyte migration in vitro and in wounded skin

Michael Meyer, Anna Katharina Müller, Jingxuan Yang, Daniel Moik, Gilles Ponzio, David M. Ornitz, Richard Grose, Sabine Werner

Research output: Contribution to journalArticlepeer-review

69 Scopus citations

Abstract

Efficient wound repair is essential for the maintenance of the integrity of the skin. The repair process is controlled by a variety of growth factors and cytokines, and their abnormal expression or activity can cause healing disorders. Here, we show that wound repair is severely delayed in mice lacking fibroblast growth factor receptors (FGFR) 1 and 2 in keratinocytes. As the underlying mechanism, we identified impaired wound contraction and a delay in re-epithelialization that resulted from impaired keratinocyte migration at the wound edge. Scratch wounding and transwell assays demonstrated that FGFR1/2-deficient keratinocytes had a reduced migration velocity and impaired directional persistence owing to inefficient formation and turnover of focal adhesions. Underlying this defect, we identified a significant reduction in the expression of major focal adhesion components in the absence of FGFR signaling, resulting in a general migratory deficiency. These results identify FGFs as key regulators of keratinocyte migration in wounded skin.

Original languageEnglish
Pages (from-to)5690-5701
Number of pages12
JournalJournal of cell science
Volume125
Issue number23
DOIs
StatePublished - Dec 2012

Keywords

  • FGF
  • Focal adhesion
  • Migration
  • Re-epithelialization
  • Wound

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