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TGF-beta1 regulates TGF-beta1 and FGF-2 mRNA expression during fibroblast wound healing
Q H Song1, V E Klepeis, M A Nugent
1Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Molecular Pathology : MP
|May 29, 2002
Summary
Transforming growth factor beta1 (TGF-beta1) enhances corneal stromal cell responsiveness and migration after injury. Fibroblast growth factor 2 (FGF-2) inhibits TGF-beta1 expression, suggesting an integral relationship during wound repair.
Area of Science:
- Cell biology
- Wound healing research
- Molecular biology
Background:
- Heparan sulfate proteoglycans and FGF-2 are transiently present during wound repair.
- TGF-beta1 mRNA increases rapidly after injury.
- Stromal cells play a role in wound repair.
Purpose of the Study:
- To evaluate the mRNA expression of TGF-beta1 and FGF-2 in corneal stromal cells post-injury.
- To investigate the effects of exogenous TGF-beta1 and FGF-2 on stromal cell mRNA expression.
- To understand the interplay between TGF-beta1 and FGF-2 during wound healing.
Main Methods:
- Primary corneal fibroblasts were cultured and subjected to injury in the presence of TGF-beta1 or FGF-2.
- mRNA expression was analyzed using northern blot and in situ hybridization.
- Dose-dependent, time-course, and whole-eye organ culture experiments were performed.
Main Results:
- Exogenous TGF-beta1 and injury increased TGF-beta1 mRNA expression and stability.
- FGF-2 inhibited TGF-beta1 expression but did not affect TGF-beta1 mRNA stability.
- Stromal cells acquired a migratory phenotype in response to growth factors.
Conclusions:
- TGF-beta1 enhances cellular responsiveness and promotes a migratory phenotype in corneal stromal cells after injury.
- FGF-2 inhibits TGF-beta1 expression, indicating a complex interaction.
- TGF-beta1 and FGF-2 have an integral relationship during the corneal wound repair process.
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