Influence of Transforming Growth Factors beta 1 and beta 3 in the Scar Formation Process.

Abstract

Transforming growth factor-beta (TGF-β) plays an instrumental role in forming scars and keloids. TGF-β isoforms exhibit differential expression, indicating distinct wound healing and scar formation functions. However, the role of TGF-β1 and TGF-β3 in wound healing and scar formation remains unclear. This study aimed to compare the specific roles of TGF-β1 and TGF-β3 in wound healing and scar formation by biomolecular analysis. The study was conducted by cell isolation and culture cells from a total of 20 human samples. Normal human fibroblasts (NHF) were isolated from normal human samples and myofibroblasts from the different scar types, namely hypertrophic (HT) and keloid (K) scars. NHF and cells from the HT, and K scar, each of which were divided into 3 sample groups: the untreated control, TGF-β1 (10µg/mL)-treated group, and TGF-β3 (10µg/mL)-treated group. The results of confocal microscopy and fluorescence-activated cell sorting experiments were compared. Both the HT and K groups had higher α-smooth muscle actin (α-SMA) expression than the NHF group in the untreated control group. In comparison with the untreated group, NHFs showed a significant increase in α-SMA expression in the TGF-β1-treated group. HT showed a high α-SMA level, which was statistically significant compared with the normal fibroblasts. In the TGF-β3-treated group, α-SMA expression was slightly increased in NHF as compared with the untreated group. TGF-β3 treated HT exhibited a greater reduction in α-SMA expression than in the TGF-β1 treated HT. K, on the other hand, had only a minimal effect on the treatment of TGF-β1 and TGF-β3. The findings suggest that TGF-β3 may play a regulatory role in the wound repair process, which could be useful in the development of scar-reducing therapies for patients with scar-related cosmetic concerns.