Abstract
Recent investigations from several laboratories, including our own, have demonstrated that the skin has the capacity to produce corticotropin-releasing factor (CRF) and proopiomelanocortin (POMC) peptides and that it can express the corresponding receptors (CRF-R and MC-R). Ultraviolet (UV) irradiation and administration of proinflammatory cytokines have been reported to increase the expression of the genes for CRF and POMC in cultured keratinocytes and melanocytes. UV irradiation of the whole body is also known to increase the level of circulating POMC peptides in the blood. In addition, administration of CRF has been found to promote production of POMC peptides and corticosteroids simultaneously in cultured melanocytes and fibroblasts. Based on these observations, it has been postulated that a system equivalent to the hypothalamicpituitary-adrenal axis might operate locally in the skin as a coordinator and executor of peripheral responses to stress. We found that systemic stress (foot shock stress and psychological stress) aggravated contact dermatitis in rat skin, prolonged the telogen stage, and delayed the subsequent anagen induction in the murine hair cycle. It is noteworthy that these effects were mediated by the actions of CRF in the skin. Therefore we propose that the skin contributes to maintaining homeostasis of the living body through its own stress response system and that CRF is a key factor of modifying cutaneous function under systemic stress conditions.
