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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothesis is presented that human emotional state is influenced by epidermal pathology via the release from epidermal keratinocytes of a wide variety of chemical mediators (including neurotransmitters) that act on the brain. It has long been recognized that epidermal keratinocytes play a key role in the function of the stratum corneum as an impermeable barrier, and that skin diseases such as atopic dermatitis and psoriasis, which cause itching, sleep disturbance and concern over appearance, are associated with depression and anxiety. On the other hand, epidermal keratinocytes are known to produce and release multiple cytokines and chemical mediators in response to barrier impairment or insult, such as environmental dryness or UV radiation. Elevation of plasma cytokines is associated with depression in cancer patients. Serum levels of oxytocin and glucocorticoid have been shown to influence mental state, and a recent study showed that glucocorticoid is generated in injured epidermis. Thus, there are multiple plausible pathways through which changes in skin can affect emotional state.
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PMID:How does epidermal pathology interact with mental state? 2324 5

The neuropeptide hormone oxytocin (OXT) mediates a wide spectrum of tissue-specific actions, ranging from cell growth, cell differentiation, sodium excretion to stress responses, reproduction and complex social behaviour. Recently, OXT expression was detected in keratinocytes, but expression of its receptor and function are still unexplored in human skin. Here, we showed that both OXT and its receptor are expressed in primary human dermal fibroblasts and keratinocytes. OXT-induced dose-dependent calcium fluxes in both cell types demonstrating that the OXT receptor (OXTR) is functionally expressed. We also showed that OXT decreases proliferation of dermal fibroblasts and keratinocytes in a dose-dependent manner. In order to further investigate OXT-mediated functions in skin cells, we performed OXTR knockdown experiments. OXTR knockdown in dermal fibroblasts and keratinocytes led to elevated levels of reactive oxygen species and reduced levels of glutathione (GSH). Moreover, OXTR-depleted keratinocytes exhibited an increased release of the pro-inflammatory cytokines IL6, CCL5 and CXCL10. Our data indicate that the OXT system modulates key processes which are dysregulated in atopic dermatitis (AD) such as proliferation, inflammation and oxidative stress responses. Furthermore, we detected a downregulation of the OXT system in peri-lesional and lesional atopic skin. Taken together, these data suggest that the OXT system is a novel neuroendocrine mediator in human skin homoeostasis and clinically relevant to stressed skin conditions like AD.
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PMID:Oxytocin modulates proliferation and stress responses of human skin cells: implications for atopic dermatitis. 2371 Oct 64