In situ hybridization for decorin and transforming growth factor-beta-1 mRNA in hypertrophic scar

Hypertrophic scar (HSc) is a fibroproliferative disorder which occurs after thermal and other injuries which penetrate the dermis. It is characterized by a perturbation in the balance of extracellular matrix components and thus an abnormal composition and organization of the matrix.; The proteoglycan decorin is abundant in normal skin and is believed to be necessary for the proper morphology of collagen fibers. Its impact in wound healing may be considerable because of its ability to bind to and neutralize the cytokine transforming growth factor-beta 1 (TGF-{dollar}beta{dollar}1). Studies of HSc have shown decorin to be virtually absent.; In contrast, systemic and local levels of TGF-{dollar}beta{dollar}1 increase after wounding in patients who develop HSc. TGF-{dollar}beta{dollar}1 is an inflammatory and fibrogenic cytokine which upregulates the production of many extracellular matrix components and inhibits the degradation of others. It can also inhibit the production of decorin through a TGF-{dollar}beta{dollar}1 negative regulatory element in the promoter of the decorin gene.; The altered amounts of decorin and TGF-{dollar}beta{dollar}1 in HSc have not been explained. In this study the patterns of expression of decorin and TGF-{dollar}beta{dollar}1 mRNAs were investigated in post-burn hypertrophic scar, post-burn mature scar and normal skin by in situ hybridization using cRNA probes labeled with digoxigenin-11-UTP.; Decorin mRNA was virtually absent in scars obtained less than 12 months after injury. A significantly higher percentage of cells expressed this mRNA between 12 and 36 months. This level of staining showed a notable reduction in specimens obtained after 36 months. All samples of normal skin studied had a very small percentage of positive cells.; The results of probing for TGF-{dollar}beta{dollar}1 were inconclusive. Preliminary analysis suggests the existence of an endogenous TGF-{dollar}beta{dollar}1 antisense transcript which may play a role in the regulation of this cytokine. (Abstract shortened by UMI.)...