Keloids represent a pathological response to cutaneous injury, creating dis
figuring scars with no known satisfactory treatment. They are characterized
by an excessive accumulation of extracellular matrix, especially collagen.
Transforming growth factor beta (TGF-P) has been implicated in the pathoge
nesis of keloids. The three TGF-P isoforms identified in mammals (TGF-beta
1, -beta 2, and -beta 3), are thought to have different biological activiti
es in wound healing. TGF-beta 1 and TGF-beta 2 are believed to promote fibr
osis and scar formation, whereas TGF-beta 3 has been shown to be either sca
r inducing or reducing, depending on the study. The aim of this study was t
o characterize expression of TGF-P isoforms in keloids at the protein level
using Western blot analysis. The authors found that TGF-beta 1 and -beta 2
proteins were at higher levels in keloid fibroblast cultures compared with
normal human dermal fibroblast cultures. In contrast, the expression of TG
F-beta 3 protein was comparable in both the normal (N = 3) and keloid (N =
3) cell lines. These findings, demonstrating increased TGF-beta 1 and -beta
2 protein expression in keloids relative to normal human dermal fibroblast
s further support the roles of TGF-beta 1 and -beta 2 as fibrosis-inducing
cytokines.