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TGF-beta2 activates proliferative scar fibroblasts.

P Smith¹, G Mosiello, L Deluca

¹Bay Pines Veterans Medical Center, Institute of Tissue Regeneration, Repair, and Rehabilitation, Bay Pines, Florida, 33744, USA.

The Journal of Surgical Research

|March 26, 1999

Summary

Transforming growth factor beta 2 (TGF-beta2) stimulates scar fibroblast contraction, but TGF-beta2 antibodies can reverse this effect. This suggests a potential therapeutic strategy for proliferative scars.

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Area of Science:

Cell Biology
Dermatology
Wound Healing Research

Background:

Cytokines, including transforming growth factor beta (TGF-beta) isoforms, are implicated in proliferative scar formation.
This study investigates the impact of exogenous TGF-beta2 on keloid, hypertrophic scar, and normal skin fibroblasts.

Purpose of the Study:

To examine the stimulating effects of TGF-beta2 on different fibroblast types in vitro.
To determine if TGF-beta2 antibody can suppress these stimulating effects.

Main Methods:

Fibroblast-populated collagen lattices (FPCLs) were used to measure fibroblast activation via lattice contraction.
Primary fibroblasts from keloids, hypertrophic scars, and normal skin were cultured and treated with TGF-beta2.
The effect of TGF-beta2 antibody on TGF-beta2-treated FPCLs was assessed over 5 days.

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Main Results:

Keloid fibroblasts exhibited the most significant response to exogenous TGF-beta2.
Normal skin fibroblasts showed delayed but significant contraction increases over time.
TGF-beta2 antibody inhibited keloid and hypertrophic scar fibroblast activity and reversed TGF-beta2-induced contraction.

Conclusions:

In vitro, TGF-beta2 antibody effectively reverses TGF-beta2-induced fibroblast contraction in proliferative scars.
These findings suggest TGF-beta2 antibody as a potential therapeutic agent for disfiguring scar conditions.