Here, we show that both, OXT and its receptor, are expressed in primary human skin cells. OXT induces dose-dependent calcium-fluxes in dermal fibroblasts and keratinocytes, indicating that the OXT receptor (OXTR) is functionally expressed in both cell types. In order to investigate potential OXT-mediated functions in skin stress responses, we performed OXTR-knockdown experiments. OXTR-knockdown in dermal fibroblasts and keratinocytes lead to elevated levels of reactive oxygen species and reduced levels of glutathione. In keratinocytes, an increased release of proinflammatory cytokines, such as IL-6, RANTES, and CXCL10 was observed.
In conclusion, atopic dermatitis, a multifactorial inflammatory skin disease, is characterized, among others, by an increased susceptibility to oxidative stress. We detected a reduced expression of the OXT system in lesional and peri-lesional atopic skin suggesting a clinical relevance in skin homeostasis.