Abstract
A series of studies has shown that application of transforming growth factor beta (TGF-beta) to a wound has a beneficial effect, especially in animals with wound healing disorders. In this study we have investigated the regulation of TGF-beta1, beta2, and beta3 and their receptors during the repair process. We found a large induction of all three TGF-beta isoforms and also of TGF-beta types I and II receptors, although the time course of induction and the absolute expression levels were different for these genes. Furthermore, each TGF-beta isoform had distinct sites of expression in the wound. Systemic treatment with glucocorticoids significantly altered the expression levels of TGF-betas and TGF-beta receptors. Whereas expression of TGF-beta1, TGF-beta2, and TGF-beta type II receptor was suppressed by glucocorticoids in normal and wounded skin, expression of TGF-beta3 and TGF-beta receptor type I mRNA was stimulated. These findings provide an explanation for the beneficial effect of exogenous TGF-beta 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- beta isoforms and their receptors might underlie the wound healing defect seen in glucocorticoid-treated animals.
Highlights
Sion of extracellular matrix proteins and integrins [7, 10]
transforming growth factor  (TGF-)3 mRNA could only be detected in the dermis, at much lower levels compared with the other types of TGF- (Fig. 1C)
Wound healing is a highly organized process that is regulated by a wide variety of growth factors and cytokines
Summary
Sion of extracellular matrix proteins and integrins [7, 10]. they have the properties expected of wound cytokines. The differential expression of TGF-s in the wound and in many embryonic mouse tissues [11, 12] suggested differential regulation of these genes and different functions of their gene products This was confirmed in in vitro studies where several differences in the potency and biological activity of TGF-1, 2, and 3 have been demonstrated. Whereas increased expression of TGF-1 and TGF-2 might have deleterious effects on the repair process by increasing scar formation, reduced expression of growth factors in a wound might result in a severe delay in wound healing This has recently been demonstrated for keratinocyte growth factor, a member of the fibroblast growth factor family, which is expressed at significantly reduced levels during wound repair in genetically diabetic db/db mice [15] and glucocorticoid-treated mice [16]. These data suggest that aberrant expression of these genes in glucocorticoid-treated mice might be associated with the wound healing defect seen in these animals
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
