The psoriatic skin resembles wound healing, and it shows abnormalities at the basement
membrane (BM), also in the non-lesional skin. Fibroblast-derived dermal periostin
has well-known functions in wound healing and Th2-mediated diseases, such as atopic
dermatitis. Here we show that serum periostin level was elevated in psoriatic patients,
remarkably in the systemically treated ones. Obvious periostin positivity was detected
in basal keratinocytes of the non-lesional, lesional, and previously-lesional psoriatic
vs. healthy skin. Ex vivo skin models were generated to examine how different skin
injuries affect periostin expression during wound healing. Our newly developed cultured
salt-split model demonstrated that BM-injury induced periostin expression in basal
keratinocytes, and periostin levels in the supernatant were also increased upon healing.
In wound healing models, β1-integrin expression was similarly induced. β1-integrin
blocking caused reduced periostin expression in in vitro scratch assay, indicating
that β1-integrin can mediate periostin production. In contrast to atopic dermatitis,
psoriatic basal keratinocytes are in an activated state and show a stable wound healing-like
phenotype with the overexpression of periostin. This abnormal BM-induced wound healing
as a potential compensatory mechanism can be initiated already in the non-lesional
skin present in the lesion and keratinocytes can remain activated in the healed skin.
