Transforming Growth Factors 
1, 
2, and 
3 and Their Receptors Are Differentially Regulated during Normal and Impaired Wound Healing (*)
- ¶ To whom correspondence should be addressed. Tel.: 089-8578-2269/2271; Fax: 089-8578-2814.
Abstract
A series of studies has shown that application of transforming growth factor β (TGF-β) to a wound has a beneficial effect, especially in animals with wound healing disorders. In this study we have investigated the regulation of TGF-β1, β2, and β3 and their receptors during the repair process. We found a large induction of all three TGF-β isoforms and also of TGF-β types I and II receptors, although the time course of induction and the absolute expression levels were different for these genes. Furthermore, each TGF-β isoform had distinct sites of expression in the wound. Systemic treatment with glucocorticoids significantly altered the expression levels of TGF-βs and TGF-β receptors. Whereas expression of TGF-β1, TGF-β2, and TGF-β type II receptor was suppressed by glucocorticoids in normal and wounded skin, expression of TGF-β3 and TGF-β receptor type I mRNA was stimulated. These findings provide an explanation for the beneficial effect of exogenous TGF-β in the treatment of impaired wound healing in glucocorticoid-treated animals. Furthermore, they suggest that a disturbed balance between the levels of the three TGF-β isoforms and their receptors might underlie the wound healing defect seen in glucocorticoid-treated animals.
Footnotes
-
↵§ Recipient of a postdoctoral fellowship from the Ernst Schering Research Foundation.
-
↵* This work was supported in part by a grant from the Bundesministerium für Bildung und Forschung (to S. W.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore by hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
-
↵1 The abbreviation used is:
- TGF-β
-
transforming growth factor β.
-
↵2 M. Madlener, unpublished data.
-
- Received October 30, 1995.
- Revision received February 9, 1996.
