Our results suggest that the low expression of miR-31 in DMSCs in patients with psoriasis causes an increase in the expression of some of its target genes, which in turn facilitates T lymphocyte activation by inhibiting the proliferation of DMSCs and therefore participates in the pathogenesis of psoriasis.
Apparently, upregulation of miR-31/miR-203 and downregulation of hsa-miR-99a/miR-125b work together in concert to facilitate the development of psoriasis pathogenesis.
The microRNA miR-31 is one of the major microRNAs in many cutaneous conditions associated with activated keratinocytes, such as the hyperproliferative diseases psoriasis, non-melanoma skin cancer and hair follicle growth. miR-31 is a marker of the hair growth phase, and in our miR-31 transgenic mouse model it impairs the function of keratinocytes.