Hypertrophic scar (HTS) represents the dermal equivalent of fibroproliferative disorders. Fibroblasts from the deep dermis are implicated in the development of HTS after
injuries that involve deeper areas of the skin. However, fibroblasts that reside in the superficial layer of the skin show antifibrotic properties, and
injuries limited to this area heal with little or no
scarring. Previously, cellular and molecular characteristics of superficial fibroblasts and deep dermal fibroblasts that may influence HTS formation were analyzed. In this study, differences in cellular behavior between superficial fibroblasts and deep dermal fibroblasts that may also affect the development of HTS or tissue
fibrosis were further characterized. Immunostaining and migration, adhesion, apoptosis, and cell viability assays were performed in fibroblasts from the superficial and deep dermis. Reverse-transcription polymerase chain reaction was used to examine the gene expression of molecules involved in cell death
after treatment of fibroblasts with
decorin. When compared with superficial fibroblasts, deep dermal fibroblasts showed lower migration rates. Although all the fibroblasts tested showed no difference in adhesion to
fibronectin, superficial fibroblasts demonstrated increased apoptotic and dead cells when treated with
decorin.
Decorin resulted in a significant increase in the expression of apoptosis markers, histone-1, caspase-1,
caspase-8, and p53 in superficial fibroblasts when compared with deep dermal fibroblasts. Taken together, the findings suggest that reduced migration, lack of
decorin, and resistance of deep dermal fibroblasts to
decorin-induced apoptosis may result in hypercellularity in
injuries involving the deep dermis, leading to deposition of excess extracellular matrix and HTS formation.