Document Detail

TGF-beta1 alters the healing of cutaneous fetal excisional wounds.
MedLine Citation:
PMID:  10359166     Owner:  NLM     Status:  MEDLINE    
BACKGROUND/PURPOSE: In a number of species, fetal wound healing differs from the adult in the absence of inflammation, fibrosis, scar formation, and excisional wound contraction. The lack of inflammation also may explain the relative absence of any cytokine levels at the wound site, such as transforming growth factor (TGF)-beta, and therefore the unique characteristics of fetal wound healing. The authors hypothesized that exogenous TGF-beta1 would induce contraction, inflammation, fibrosis, and scar formation in cutaneous excisional wounds in the fetal rabbit. METHODS: Cellulose discs (3 mm in diameter) were formulated with either 1.0 microg TGF-beta1 (n = 6) or bovine serum albumin (BSA; n = 7), as a control, for sustained-release over 3 days. Each disc was implanted into the subcutaneous tissue on the backs of fetal New Zealand White Rabbits in utero on day 24 of gestation (term, 31 days). A full-thickness, 3-mm excisional wound (7.4 mm2) was then made next to the implanted cellulose disc. All wounds were harvested 3 days later. RESULTS: At harvest, the excisional wounds in the TGF-beta1 group had contracted (5.6 +/- 2.0 mm2), whereas those in the control group had expanded (13.5 +/- 1.2 mm2, P< .01). The surrounding dermis in the TGF-beta1 group had 16.3 inflammatory cells per grid block compared with 12.4 cells in the control group (not significant). In addition, a greater amount of fibrosis was induced by the TGF-beta1 implant (1.7 +/- 0.3) than the control implant (0.4 +/- 0.2) on a scale of 0 to 3, P < .01. In situ hybridization analysis showed an increase in procollagen type 1alpha1 gene expression in the surrounding dermis of the TGF-beta1 group (36.7 +/- 3.6 grains per grid block) compared with the control group (7.1 +/- 0.9 grains per grid block, P < .001). CONCLUSIONS: These results demonstrate that the cytokine TGF-beta1 can induce fetal excisional wounds to contract, stimulate fibrosis, and increase procollagen type 1alpha1 gene expression. These findings further suggest that the absence of TGF-beta1 atthe wound site may be responsible in part for the lack of a postnatal healing response.
D A Lanning; B C Nwomeh; S J Montante; D R Yager; R F Diegelmann; J H Haynes
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of pediatric surgery     Volume:  34     ISSN:  0022-3468     ISO Abbreviation:  J. Pediatr. Surg.     Publication Date:  1999 May 
Date Detail:
Created Date:  1999-07-15     Completed Date:  1999-07-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0052631     Medline TA:  J Pediatr Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  695-700     Citation Subset:  IM    
Medical College of Virginia/Virginia Commonwealth University, Richmond 23298, USA.
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MeSH Terms
Collagen / metabolism
Fetus / physiology*
Gene Expression
In Situ Hybridization
Transforming Growth Factor beta / physiology*
Wound Healing / physiology*
Grant Support
Reg. No./Substance:
0/Transforming Growth Factor beta; 9007-34-5/Collagen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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