Improving stretch mark pathophysiology knowledge by specific in vitro models



Common during pregnancy, stretch marks or Striae Distensae (SD) result from many factors and look like atrophied scars. Despite their frequency, the physiopathogenic pathways involved in their formation are not fully understood. The dermal fibroblast is the target cell under biomechanical and hormonal influences.
In order to improve our understanding of the mechanisms involved in SD development, we developed several in vitro study models.
We used normal dermal fibroblasts under different treatment conditions mimicking mechanical distension or hormonal environment, as well as fibroblasts isolated from SD, and study their behaviour and synthesis potential.
Fibroblasts exposed to TGFβ1 transformed to myofibroblasts. Corticosteroids inhibited their secretion of collagen 1. Scratch-assay coupled with TGFβ1 or corticosteroid demonstrated opposite results on proliferation.
SD fibroblasts exerted a stronger contractile force under tension than classic ones. Their protein synthesis was decreased (collagen 1 and 3 -20%, fibronectin -14% and elastin -16%).
Whole-transcriptome analysis of SD fibroblasts compared to normal fibroblasts from the same donors tended to demonstrate increased inflammation and elastin degradation factors as well as altered repair process.
To go further, we used a specific model that mimics extra-cellular matrix changes as they occur in the stretch marks formation: a dermal injury was conducted on a full-thickness skin model. The injury induced a decrease in collagen I, VII, elastin and beta1-integrin gene expression.
These in vitro models allowed us to understand the different phases involved in SD formation, they provide useful tools to evaluate the biological properties of active ingredients and anti-stretch marks topical products.


Ms Gaelle Bellemere