Journal
PHARMACEUTICAL RESEARCH
Volume 20, Issue 3, Pages 345-350Publisher
KLUWER ACADEMIC/PLENUM PUBL
DOI: 10.1023/A:1022635600479
Keywords
gene transfer; TGF-beta 1; diabetics; wound healing
Funding
- NCI NIH HHS [CA74918] Funding Source: Medline
- NIAID NIH HHS [AI48851] Funding Source: Medline
- NIAMS NIH HHS [AR45925] Funding Source: Medline
- NIDDK NIH HHS [DK54225] Funding Source: Medline
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Purpose. To evaluate the biologic effect of direct cutaneous TGF-beta1 gene delivery on impaired wound healing models using genetically diabetic mice. Methods. Diabetic mice (C57BKS. Cg-m +/+ Leprdb female mice) with 1 cm x 1 cmexcisional wounds were intradermally injected with 60 mug of plasmid DNA encoding TGF-beta1 gene. The wound closure was measured up to 14 days postwounding. At days 7 and 14 postwounding, sections of skin were taken for hematoxylin and eosin and Masson's trichome staining to examine the morphology and collagen deposition. The cell proliferation and TGF-beta1 gene expression were studied using immunohistochemical stainings for 5-bromo-2-deoxyuridine and for TGF-beta1. Results. A higher cell proliferation rate and a denser and more organized new extracellular matrix were observed in the treated wound site. Complete wound closure was detected as early as 7 days for TGF-beta1-treated group in comparison with 11-14 days for the untreated, control plasmid DNA- and PBS-treated groups. Conclusion. A single intradermal injection of TGF-beta1 plasmid DNA was sufficient to enhance wound healing. This approach represents a new strategy that may be applied to the treatment of excisional wounds in human diabetic patients.
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