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Updated: May 11, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

Effects of botulinum toxin type A on expression of genes in keloid fibroblasts

Wang Xiaoxue1, Chen Xi, Xiao Zhibo

  • 1Second Affiliated Hospital of the Harbin Medical University, Harbin City, China.

Aesthetic Surgery Journal
|May 28, 2013
PubMed
Abstract

Insights

Botulinum toxin type A (BoNT-A) alters gene expression in keloid fibroblasts, downregulating key growth factors like TGF-β1 and VEGF. This finding offers insights into BoNT-A's mechanism for treating keloid scars.

Area of Science:

  • Dermatology and Molecular Biology

Background:

  • Keloid scars involve invasive fibroblast growth, a process influenced by various biological factors.
  • Botulinum toxin type A (BoNT-A) shows potential in inhibiting keloid invasive growth, but its molecular mechanisms require elucidation.

Purpose of the Study:

  • To investigate the impact of BoNT-A on the expression of genes associated with invasive growth in keloid fibroblasts.

Main Methods:

  • Microarray analysis was employed to assess messenger RNA expression profiles of 112 genes related to invasive growth in BoNT-A-treated keloid fibroblasts.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to validate the microarray findings.

Main Results:

  • BoNT-A treatment led to the upregulation of the S100A4 gene.
  • Conversely, BoNT-A downregulated the expression of TGF-β1, VEGF, MMP-1, and PDGFA genes in keloid fibroblasts.

Conclusions:

  • The observed alterations in S100A4, TGF-β1, VEGF, MMP-1, and PDGFA gene expression by BoNT-A provide valuable insights into its functional role.
  • These findings suggest potential novel therapeutic strategies for keloid scarring by targeting these specific genes.
Keywords:
botulinum toxin type Afibroblastgene expressioninvasive growthkeloidresearch

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