Background: Psoriasis is characterized by chronic inflammatory dermatosis, and the pathogenesis of psoriasis is associated with mesenchymal stem cells (MSCs) and deregulation of the expression of miR-31. This study aimed to clarify the function of miR-31 in dermal MSCs (DMSCs) in the pathogenesis of psoriasis.
Methods: The expression of miR-31 was assayed by a microarray and that of target genes of miR-31 was tested by quantitative PCR.
Results: The expression of miR-31 in the psoriasis group was 0.2677 folds that of the control group. The expression of EMP1 and EIG121L genes, whose products are located on the cell membrane, in the psoriasis group was 4.095579 and 5.367017 folds that in the control group, respectively. The expression of GRB10, PTPN14, QKI, RNF144B, and TACC2 genes, whose products are located in the cytoplasm, in the psoriasis group was 1.440428, 1.198335, 1.737285, 7.379546, and 1.531947 folds that of the control. The expression of PRELP, whose products are secreted in the extracellular space, in the psoriasis group was 1.351684 folds that of the control. The expression of RBMS1, KHDRBS3, and SATB2, whose products play a role in the nucleus, in the psoriasis group was 2.237199, 1.277159, and 1.005742 folds that of the control, respectively.
Conclusions: 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.
© 2018 The International Society of Dermatology.