| Plasminogen activator inhibitor-I-related regulation of procollagen I (alpha1 and alpha2) by antitransforming growth factor-beta1 treatment during radiation-impaired wound healing. | |
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MedLine Citation:
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PMID: 16377416 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Plasminogen activator inhibitor (PAI)-1 mediates transforming growth factor-beta1 (TGF-beta1)-related signaling by stimulating collagen Type I synthesis in radiation-impaired wound healing. The regulation of alpha(I)-procollagen is contradictory in fibroblasts of different fibrotic lesions. It is not known whether anti-TGF-beta1 treatment specifically inhibits alpha(I)-procollagen synthesis. We used an experimental wound healing study to address anti-TGF-beta1-associated influence on alpha(I)-procollagen synthesis. METHODS AND MATERIALS: A free flap was transplanted into the preirradiated (40 Gy) or nonirradiated neck region of Wistar rats: Group 1 (n = 8) surgery alone; Group 2 (n = 14) irradiation and surgery; Group 3 (n = 8) irradiation and surgery and anti-TGF-beta1 treatment. On the 14th postoperative day, skin samples were processed for fibroblast culture, in situ hybridization for TGF-beta1, immunohistochemistry, and immunoblotting for PAI-1, alpha1/alpha2(I)-procollagen. RESULTS: Anti-TGF-beta1 significantly reduced TGF-beta1 mRNA (p < 0.05) and PAI-1 expression (p < 0.05). Anti-TGF-beta1 treatment in vivo significantly reduced alpha1(I)-procollagen protein (p < 0.05) and the number of expressing cells (p < 0.05) in contrast to significantly increased (p < 0.05) alpha2(I)-procollagen expression. CONCLUSION: These results emphasize anti-TGF-beta1 treatment to reduce radiation-induced fibrosis by decreasing alpha1(I)-procollagen synthesis in vivo. alpha1(I)-procollagen and alpha2(I)-procollagen might be differentially regulated by anti-TGF-beta1 treatment. Increased TGF-beta signaling in irradiated skin fibroblasts seemed to be reversible, as shown by a reduction in PAI-1 expression after anti-TGF-beta1 treatment. |
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Authors:
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Stefan Schultze-Mosgau; Jürgen Kopp; Michael Thorwarth; Franz Rödel; Ivan Melnychenko; Gerhard G Grabenbauer; Kerstin Amann; Falk Wehrhan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of radiation oncology, biology, physics Volume: 64 ISSN: 0360-3016 ISO Abbreviation: Int. J. Radiat. Oncol. Biol. Phys. Publication Date: 2006 Jan |
Date Detail:
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Created Date: 2005-12-26 Completed Date: 2006-03-23 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7603616 Medline TA: Int J Radiat Oncol Biol Phys Country: United States |
Other Details:
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Languages: eng Pagination: 280-8 Citation Subset: IM |
Affiliation:
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Department of Oral and Maxillofacial Surgery/Plastic Surgery, Freidrich-Schiller-University of Jena, Jena, Germany. stefan.schultze-mosgau@med.uni-jena.de |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Collagen Type I / biosynthesis* Fibroblasts / metabolism, radiation effects Male Plasminogen Activator Inhibitor 1 / metabolism, physiology* RNA, Messenger / biosynthesis Radiation Injuries / prevention & control Rats Rats, Wistar Surgical Flaps / physiology Transforming Growth Factor beta / antagonists & inhibitors*, immunology Transforming Growth Factor beta1 Wound Healing* |
| Chemical | |
Reg. No./Substance:
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0/Collagen Type I; 0/Plasminogen Activator Inhibitor 1; 0/RNA, Messenger; 0/Tgfb1 protein, rat; 0/Transforming Growth Factor beta; 0/Transforming Growth Factor beta1 |
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