Aims: We have previously shown that hypertrophic scar tissue from burn pati
ents contains abnormally high amounts of the proteoglycans versican and big
lycan and reduced amounts of decorin, in comparison with normal dermis or m
ature scar. The lack of decorin may account for the poor organization of co
llagen fibrils in the nodular areas of these scars. Decorin has also been r
eported to neutralize the fibrogenic growth factor TGF-beta 1. This study w
as conducted to monitor the time-course of expression of decorin in healing
burn wounds by in-situ hybridization to determine whether its absence from
hypertrophic scars could result from reduced synthesis.
Methods and results: Scar tissue from 19 patients and normal dermis from si
x patients, was fixed in paraformaldehyde, embedded in paraffin and section
ed. Digoxigenin-labelled cRNA probes were prepared from a plasmid containin
g a 622-bp insert of human decorin cDNA and used for in-situ hybridization.
Total numbers of connective tissue cells and cells positive for decorin mR
NA were counted in 10 random fields in the upper (papillary), middle and lo
wer (reticular) one-thirds of the dermis. In all regions the number and per
centages of cells with decorin mRNA were low during the first 12 months aft
er injury (eight samples), much higher between 12 and 36 months (seven samp
les) and low and similar to those in normal skin after 36 months (five samp
les). The differences between intermediate and early or late stage samples
were statistically significant (one-way anova). Immunohistochemistry showed
little staining for decorin in early stage samples and much stronger stain
ing in mid-stage. Late stage tissue showed intense staining for decorin, al
most comparable to that in normal dermis.
Conclusion: Expression of decorin in burn wounds is suppressed for about 12
months and then increases at a time when resolution of hypertrophic scarri
ng is generally considered to occur.