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Updated: Jun 3, 2026

In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
Botulinum toxin type a inhibits connective tissue growth factor expression in fibroblasts derived from hypertrophic
Zhibo Xiao1, Miaobo Zhang, Ying Liu
1Department of Plastic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin City, P.R. China. xiaozhibodoctor@yahoo.com.cn
Background:
Botulinum toxin type A (BTXA) can inhibit the growth of hypertrophic scars, but the molecular mechanism for this action is unknown. In addition to reducing the tension around the wound by stimulating temporary denervation, a growing body of evidence suggests that BTXA is involved in regulating the cell cycle and decreasing transforming growth factor-β1 (TGF-β1) expression in the fibroblasts of hypertrophic scars. Connective tissue growth factor (CTGF) is a downstream regulator of TGF-β1 function and an independent mediator of scarring and fibrosis. The effects of BTXA on CTGF in hypertrophic scar still are unknown. This study aimed to explore the effect of BTXA on CTGF in fibroblasts derived from hypertrophic scar and to elucidate its actual mechanism further.
Methods:
Fibroblasts isolated from tissue specimens of hypertrophic scar were treated with BTXA. The difference in proliferation between treated and nontreated fibroblasts was analyzed by flow cytometry. Proteins of CTGF were checked using Western blot in fibroblasts with and without BTXA.
Results:
The proliferation of the fibroblasts treated with BTXA was slower than that of the fibroblasts that had no BTXA treatment (p < 0.01), which showed that BTXA effectively inhibited the growth of fibroblasts. Compared with fibroblasts that received no BTXA treatment, BTXA at 1 U/10(6) cells decreased the expression of CTGF by 49.2% ± 12.5% (p < 0.01), and BTXA at 2.5 U/10(6) cells decreased the expression of CTGF by 56.9% (p < 0.01).
Conclusion:
These results suggest that BTXA effectively inhibited the growth of fibroblasts derived from hypertrophic scar and in turn caused a decrease in CTGF protein, providing theoretical support for the application of BTXA to control hypertrophic scarring.
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