Effects of Basic Fibroblast Growth Factors on Hypertrophic Scarring in a Rabbit Ear Model

Background: Basic fibroblast growth factor (bFGF) was clinically proven to accelerate acute and chronic wound healing. Accelerated wound healing may lead to improved scarring. These studies suggested a possible antiscarring effect of bFGF during wound healing. Little was known about the precise path...

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Veröffentlicht in:Journal of cutaneous medicine and surgery 2008-07, Vol.12 (4), p.155-162
Hauptverfasser: Xie, Julin, Qi, Shaohai, Xu, Yingbin, Tang, Jingming, Li, Tianzeng, Liu, Xusheng, Shu, Bin, Liang, HuiZhen, Huang, Bing
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Sprache:eng
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Zusammenfassung:Background: Basic fibroblast growth factor (bFGF) was clinically proven to accelerate acute and chronic wound healing. Accelerated wound healing may lead to improved scarring. These studies suggested a possible antiscarring effect of bFGF during wound healing. Little was known about the precise pathologic mechanisms of bFGF on scarring formation. Aims: The aim of this study was to investigate the effect of bFGF on hypertrophic scarring in a rabbit ear model and clarify the mechanism of bFGF on scar treatment. Methods: The rabbit model of hypertrophic scarring was created and received of a low- or high-dose topical treatment three times daily for 1, 2, or 3 months. Then we examined the changes in the macroscopic and histopathologic characteristics of the scars. The expression of collagen, α1β2 integrin, and matrix metalloproteinase 1 (MMP-1) was studied by applying reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blotting. Result: High-dose bFGF remarkably alleviated the scar in the rabbit ear model and decreased collagen type I expression. Further study revealed that bFGF remarkably enhanced MMP-1 and decreased α1β2 integrin expression. Conclusion: This study supports the hypothesis that bFGF exerted a net negative effect on collagen remodeling, therefore suggesting a potential antiscarring role.
ISSN:1203-4754
1615-7109
DOI:10.2310/7750.2008.07041