Upon ageing, chronic exposure to ultraviolet radiations and pollution induces benign hyper-pigmented lesions, such as Solar Lentigo maculae (SL) 1. Well-defined histologically, SL is distinguishable from other hyper-pigmented diseases and can be classified relative to its evolution 2-4. Differential gene-profiling analyses comparing SL and normal skin biopsies revealed that SL tissues are mainly composed of epidermal activated melanocytes as well as hypo-proliferating and hypo-differentiated keratinocytes with a background of chronic inflammation. In absence of fibroblast markers, immuno-staining analyses for several growth factors and secreted proteins in the upper dermis of SL biopsies strongly suggest that dermal fibroblasts contribute functionally to dysregulation of epidermal cells 5. These observations are strengthened by recent studies using a pigmented reconstructed skin model that demonstrates the influence of dermal fibroblasts on skin pigmentation 6. However, data on the morphological and functional features of the SL primary fibroblasts that could explain their role in SL disease are not available.
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