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A Human Corneal Organ Culture Model of Descemet's Stripping Only with Accelerated Healing Stimulated by Engineered Fibroblast Growth Factor 1
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Expression and function of fibroblast growth factor-inducible 14 in human corneal myofibroblasts

Nobuyuki Ebihara1, Masafumi Nakayama, Tomoko Tokura

  • 1Department of Ophthalmology, Juntendo University School of Medicine, Tokyo 113-8431, Japan. ebihara@juntendo.ac.jp

Experimental Eye Research
|April 7, 2009
PubMed

Insights

The fibroblast growth factor-inducible 14 (Fn14)/tumor necrosis factor-like weak inducer of apoptosis (TWEAK) system is expressed in corneal myofibroblasts and influences wound healing. Modulating this pathway may offer novel strategies for controlling corneal wound repair.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Tissue Repair

Background:

  • Fibroblast growth factor-inducible 14 (Fn14) and its ligand tumor necrosis factor-like weak inducer of apoptosis (TWEAK) are crucial for tissue wound healing.
  • The role of Fn14 in corneal myofibroblasts, key players in corneal stroma wound healing, remains uninvestigated.

Purpose of the Study:

  • To investigate the expression and function of Fn14 in corneal myofibroblasts.
  • To elucidate the role of the Fn14/TWEAK system in corneal wound healing processes.

Main Methods:

  • Flow cytometry was used to assess Fn14 protein expression in corneal myofibroblasts and keratocytes.
  • ELISA detected chemokines and matrix metalloproteinases (MMPs) in cultured cells.
  • Western blotting assessed TWEAK-induced signaling pathways (NF-kappaB, MAP kinase).

Main Results:

  • Corneal myofibroblasts exhibited strong Fn14 expression, unlike keratocytes. TGF-beta(1) induced Fn14 expression and myofibroblast differentiation.
  • TWEAK, via Fn14, increased IL-8, MCP-1, RANTES, and MMP-1/-3 production by myofibroblasts, with TGF-beta(1) augmenting chemokine and inhibiting MMP production.
  • TWEAK activated NF-kappaB and MAP kinase pathways and partially inhibited TGF-beta(1)-induced keratocyte differentiation.

Conclusions:

  • The Fn14/TWEAK system is expressed in corneal myofibroblasts and significantly influences their function.
  • This system plays multifaceted roles in corneal wound healing, affecting chemokine and MMP production and myofibroblast differentiation.
  • Targeting the TWEAK/Fn14 pathway presents a potential therapeutic strategy for modulating corneal wound healing.

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