Fibrillin-1 and elastin are differentially expressed in hypertrophic scars and keloids

Hypertrophic scars and keloids are two forms of excessive cutaneous scarring. Considering the importance of extracellular matrix elements in tissue repair, a morphological and quantitative analysis of the elastic system components (fibrillin‐1 and elastin) was performed in normal skin, normal scars,...

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Veröffentlicht in:Wound repair and regeneration Jg. 12; H. 2; S. 169 - 174
Hauptverfasser: Amadeu, Thaís P., Braune, André S., Porto, Luís C., Desmoulière, Alexis, Costa, Andréa M. A.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Oxford, UK; Malden, USA Blackwell Science Inc 01.03.2004
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ISSN:1067-1927, 1524-475X
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Zusammenfassung:Hypertrophic scars and keloids are two forms of excessive cutaneous scarring. Considering the importance of extracellular matrix elements in tissue repair, a morphological and quantitative analysis of the elastic system components (fibrillin‐1 and elastin) was performed in normal skin, normal scars, hypertrophic scars, and keloids. In superficial and deep dermis, fibrillin‐1 volume density was significantly higher in normal skin compared with normal scars, hypertrophic scars, and keloids. The fibrillin‐1 volume density did not show differences between hypertrophic scars and keloids in superficial or deep dermis. In superficial dermis, elastin volume density was higher in normal skin compared with normal scars, hypertrophic scars, and keloids. In deep dermis, the elastin volume density was higher in keloids compared with normal skins, normal scars, and hypertrophic scars. We showed that the distribution of fibrillin‐1 and elastin is disrupted in all kinds of scars analyzed, but there are two patterns: one for normal scars and another for excessive scars.
Bibliographie:istex:9502D480F1D5CFF80D42E45DE3C3ACEAC9C8B1BB
ark:/67375/WNG-V0RLDR8R-5
ArticleID:WRR12209
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1067-1927
1524-475X
DOI:10.1111/j.1067-1927.2004.012209.x