Fibroblast growth factor-peptide improves barrier function and proliferation in human keratinocytes after radiation

Int J Radiat Oncol Biol Phys. 2011 Sep 1;81(1):248-54. doi: 10.1016/j.ijrobp.2011.02.004. Epub 2011 Apr 12.

Abstract

Purpose: Epidermal keratinocytes, which can be severely damaged after ionizing radiation (IR), are rapid turnover cells that function as a barrier, protecting the host from pathogenic invasion and fluid loss. We tested fibroblast growth factor-peptide (FGF-P), a small peptide derived from the receptor-binding domain of FGF-2, as a potential mitigator of radiation effects via proliferation and the barrier function of keratinocytes.

Methods and materials: Keratinocytes isolated from neonatal foreskin were grown on transwells. After being exposed to 0, 5, or 10 Gy IR, the cells were treated with a vehicle or FGF-P. The permeability of IR cells was assessed by using transepithelial electrical resistance (TEER) and a paracellular tracer flux of fluorescein isothiocyanate-conjugated bovine serum albumin (FITC-BSA) with Ussing chambers. The cell proliferation was measured with yellow tetrazolium salt (MTT) and tritiated thymidine ([3H]-TdR) assays. The phosphorylation of extracellular signal-regulated kinases (ERK) was measured in an enzyme-linked immunosorbent (ELISA)-like assay, and the proteins related to tight junctions (TJ) and adherens junctions (AJ) were examined with Western blotting. We used a mouse model to assess the ability of FGF-P to promote the healing of skin β burns created with a strontium applicator.

Results: We found (1) FGF-P reduced the permeability of irradiated keratinocytes, as evidenced by increased TEER and decreased diffusion of FITC-BSA, both associated with the regulation of different proteins and levels of TJ and AJ; and (2) FGF-P enhanced the proliferation of irradiated keratinocytes, as evidenced by increased MTT activity and [3H]-TdR incorporation, which was associated with activation of the ERK pathway; and (3) FGF-P promoted the healing of skin β burns.

Conclusions: FGF-P enhances the barrier function, including up-regulation of TJ proteins, increases proliferation of human keratinocytes, and accelerates the healing of skin β burns. FGF-P is a promising mitigator that improves the proliferation and barrier function of keratinocytes after IR.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Division
  • Cell Membrane Permeability / drug effects*
  • Cell Membrane Permeability / physiology
  • Cell Membrane Permeability / radiation effects
  • Cell Proliferation
  • Drug Evaluation, Preclinical / methods
  • Electric Impedance
  • Epidermal Cells
  • Epidermis / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Fibroblast Growth Factor 2 / pharmacology*
  • Fluorescein-5-isothiocyanate / analogs & derivatives
  • Fluorescein-5-isothiocyanate / pharmacokinetics
  • Humans
  • Keratinocytes / cytology
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Keratinocytes / radiation effects
  • Male
  • Membrane Proteins / analysis
  • Mice
  • Mice, Inbred BALB C
  • Peptide Fragments / pharmacology*
  • Phosphorylation
  • Radiation Injuries, Experimental / drug therapy
  • Radiation-Protective Agents / pharmacology*
  • Random Allocation
  • Serum Albumin / pharmacokinetics
  • Tight Junctions / metabolism
  • Wound Healing / drug effects

Substances

  • FGF-P peptide
  • FITC-albumin
  • Membrane Proteins
  • Peptide Fragments
  • Radiation-Protective Agents
  • Serum Albumin
  • Fibroblast Growth Factor 2
  • Extracellular Signal-Regulated MAP Kinases
  • Fluorescein-5-isothiocyanate