Striae distensae are characterized by linear, smooth bands of atrophic-appearing skin that are reddish at first and finally white. They are due to stretching of the skin, as in rapid weight gain, or mechanical stress, as in weight lifting. The pathogenesis of striae distensae is unknown but probably relates to changes in the fibroblast phenotype. In order to characterize striae distensae fibroblasts, alpha-smooth muscle actin expression and contractile forces were studied. Five healthy women with early erythematous striae and five healthy women with older striae were selected. Paired biopsies were taken from the center of lesional striae and adjacent normal skin. Fibroblasts were obtained by an explant technique and expanded in vitro in Dulbecco's modified Eagle's medium. Contractile forces generated by fibroblasts in collagen lattices were measured with the Glasbox device developed in our laboratory. Alpha-smooth muscle actin expression was studied by immunofluorescence labeling of cells and by flow cytometry. Fibroblasts from early striae distensae were the richest cells in alpha-smooth muscle actin filaments and generated the highest contractile forces. Their peak contractile force was 26% greater than normal fibroblasts. There was a 150% higher level of alpha-smooth muscle actin content in fibroblasts from early striae distensae compared with fibroblasts from normal skin. In contrast, there was no significant difference in force generation between old striae fibroblasts and normal fibroblasts with cells expressing no alpha-smooth muscle actin. The contractile properties of fibroblasts from striae distensae varies depending on the stage of the disease. In early striae distensae, fibroblasts acquire a more contractile phenotype, corresponding to that of myofibroblasts.

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Human dermal fibroblasts seeded in tense disc-shaped collagen gels organized gradually into a tissue composed of three distinct superimposed layers of cells: a basal layer of aligned myofibroblasts, a middle layer of unoriented fibroblasts, and an upper layer of myofibroblasts oriented orthogonally to the basal myofibroblasts. Confocal observation of alpha-smooth muscle actin (alpha-SMA) immunolabelling as a marker of myofibroblasts showed that the upper myofibroblasts disappeared during maturation of the lattices. Observation of morphological modifications of cells, typical chromatin condensation identified by Hoechst 33258 staining, and detection of ssDNA after formamide-induced denaturation suggested the involvement of apoptosis in myofibroblast disappearance. It is suggested that the model of disc-shaped stressed collagen lattice is thus able to mimic conditions in wound repair: on the one hand, wound contraction during which fibroblasts undergo mechanical stress and, on the other, apoptotic disappearance of cells at the end of tissue retraction.