CONTRACTILITY, TRANSFORMING-GROWTH-FACTOR-BETA, AND PLASMIN IN FETAL SKIN FIBROBLASTS - ROLE IN SCARLESS WOUND-HEALING

Citation
C. Coleman et al., CONTRACTILITY, TRANSFORMING-GROWTH-FACTOR-BETA, AND PLASMIN IN FETAL SKIN FIBROBLASTS - ROLE IN SCARLESS WOUND-HEALING, Pediatric research, 43(3), 1998, pp. 403-409
Citations number
40
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
43
Issue
3
Year of publication
1998
Pages
403 - 409
Database
ISI
SICI code
0031-3998(1998)43:3<403:CTAPIF>2.0.ZU;2-6
Abstract
The early fetus responds to cutaneous wounds in a fundamentally differ ent way from the adult; fetal wounds heal without scars. Wound contrac tion is a vital component of wound healing. The cytokine transforming growth factor (TGF)-beta promotes wound contraction and can be activat ed by the serine protease plasmin. Herein, we explored whether murine skin fibroblast contractile properties, TGF-beta, and plasmin formatio n are developmentally regulated. Our results showed that early fetal m ouse embryonic day 15 skin fibroblasts contracted a collagen gel less, secreted less active and total TGF-beta, and generated less plasmin t han either late fetal (embryonic day 17) or adult skin fibroblasts. Fu rthermore, there was a slight positive correlation between the formati on of plasmin and the level of activation of TGF-beta. We conclude tha t early fetal mouse skin fibroblasts contract a collagen gel and secre te and activate TGF-beta to a lesser extent than do late fetal and adu lt skin fibroblasts. We speculate that the fetal skin fibroblast under goes a developmental transition that causes wounds in mouse to contrac t at or after embryonic day 17., Further, this developmental transitio n is influenced by growth factor-fibroblast interactions and coincides with the emergence of the skin fibroblast's ability to generate plasm in and activate TGF-beta.