A possible mechanism of basic fibroblast growth factor-promoted scarless wound healing: The induction of myofibroblast apoptosis

  • Abe M
  • Yokoyama Y
  • Ishikawa O
  • 20

    Readers

    Mendeley users who have this article in their library.
  • 32

    Citations

    Citations of this article.

Abstract

Although recent clinical reports have indicated that recombinant basic fibroblast growth factor (bFGF) promotes scarless wound healing, the mechanism remains unclear. The present study was carried out to elucidate the mechanisms. The protein levels of cellular α-smooth muscle actin increased at 2-4 days after TGFβ treatment alone and at 4 to 6 days after a costimulation of bFGF and TGFβ. A spontaneous contraction of stressed myofibroblast-collagen matrix was cancelled by bFGF, which was restored under the presence of C3 exotransferase or Y27632. bFGF stimulation of myofibroblasts as well as fibroblasts elicited a transient Rac and Rho activation. bFGF promoted apoptosis of the myofibroblasts but not of the fibroblasts, even in the presence of two different inhibitors, either LY294002 or an Akt inhibitor. The present study suggests that the phosphatidylinositol-3-kinase to Akt as well as the Rho to Rho kinase signaling pathway is involved in bFGF-promoted myofibroblast apoptosis, and bFGF can promote the scarless wound healing upon the induction of apoptosis of myofibroblasts, but not fibroblasts.

Author-supplied keywords

  • Akt
  • Apoptosis
  • Basic fibroblast growth factor (bFGF)
  • Rho family
  • Scarless wound healing

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • Masatoshi Abe

  • Yoko Yokoyama

  • Osamu Ishikawa

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free