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Efficacy and possible mechanisms of Botulinum Toxin type A on hypertrophic scarring
Author(s) -
Hao RongTao,
Li ZongChao,
Chen Xing,
Ye Wei
Publication year - 2018
Publication title -
journal of cosmetic dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.626
H-Index - 44
eISSN - 1473-2165
pISSN - 1473-2130
DOI - 10.1111/jocd.12534
Subject(s) - keloid , hypertrophic scar , fibroblast , viability assay , apoptosis , medicine , blot , botulinum toxin , cell cycle , flow cytometry , cancer research , chemistry , pathology , surgery , immunology , biochemistry , in vitro , gene
Summary Background Clinical observations indicate that Botulinum toxin type A ( BTXA ) can inhibit the growth and improve the eventual appearance of hypertrophic scarring. However, the molecular mechanism remains unclear. Objective We used human keloid fibroblasts to investigate the molecular mechanism of BTXA on hypertrophic scarring. Methods Different concentrations of BTXA (0.01, 0.1, 1, and 10 U/L) were used to treat keloid fibroblasts. Changes in cellular morphology, viability, proliferation, cell cycle, and apoptosis were observed by immunofluorescence, MTT assay, and flow cytometry. In addition, real‐time qPCR and Western blotting were used to explore the potential molecular mechanisms. Results Keloid fibroblast viability decreased with increasing BTXA dose. After BTXA treatment, the volume of keloid fibroblasts cells increased, but the nucleus of cells shrunk. Long thin dendrites were formed as the concentration of BTXA increased. Furthermore, the proliferation and S phase of keloid fibroblasts were inhibited by BTXA . Matrix metalloproteinase (, MMP )‐1 and ‐2 RNA and protein showed high expression, but TGF ‐β1 and MMP ‐9 showed low expression than the control. Conclusion Botulinum toxin type A may promote the healing of scars by inhibiting the proliferation of keloid fibroblasts and regulating the expression of TGF ‐β1, which could affect the expression of MMP ‐1 and MMP ‐2. This study provides theoretical support for the clinical application of BTXA to control hypertrophic scarring.

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