Abstract
Human scalp skin and hair follicles (HFs) are extra-pituitary sources of prolactin (PRL). However, the intracutaneous regulation of PRL remains poorly understood. Therefore we investigated whether well-recognized regulators of pituitary PRL expression, which also impact on human skin physiology and pathology, regulate expression of PRL and its receptor (PRLR) in situ. This was studied in serum-free organ cultures of microdissected human scalp HFs and skin, i.e. excluding pituitary, neural and vascular inputs. Prolactin expression was confirmed at the gene and protein level in human truncal skin, where its expression significantly increased (p = 0.049) during organ culture. There was, however, no evidence of PRL secretion into the culture medium as measured by ELISA. PRL immunoreactivity (IR) in female human epidermis was decreased by substance P (p = 0.009), while neither the classical pituitary PRL inhibitor, dopamine, nor corticotropin-releasing hormone significantly modulated PRL IR in HFs or skin respectively. Interferon (IFN) γ increased PRL IR in the epithelium of human HFs (p = 0.044) while tumour necrosis factor (TNF) α decreased both PRL and PRLR IR. This study identifies substance P, TNFα and IFNγ as novel modulators of PRL and PRLR expression in human skin, and suggests that intracutaneous PRL expression is not under dopaminergic control. Given the importance of PRL in human hair growth regulation and its possible role in the pathogenesis of several common skin diseases, targeting intracutaneous PRL production via these newly identified regulatory pathways may point towards novel therapeutic options for inflammatory dermatoses.
Highlights
Whilst prolactin (PRL) is appreciated for its role in the modulation of hair growth, both in human and other mammalian species [1,2], less attention has been afforded to the role(s) of PRL in cutaneous biology and pathology in general
Given the pro-inflammatory cutaneous cytokine milieu which is present in psoriasis, we speculated that cytokines, for example tumour necrosis factor alpha (TNFa) and interferon gamma (IFNc), may up-regulate intracutaneous PRL production
Since pituitary PRL secretion may be regulated by IFNc and TNFa, albeit in rodent studies [46,47,48,49], and since these cytokines [50,51] and PRL [3,5,28,52,53] have been implicated in the pathogenesis of psoriasis, we examined whether these prototypic pro-inflammatory cytokines influence PRL and PRL and its receptor (PRLR) expression in the hair follicles (HFs)
Summary
Whilst prolactin (PRL) is appreciated for its role in the modulation of hair growth, both in human and other mammalian species [1,2], less attention has been afforded to the role(s) of PRL in cutaneous biology and pathology in general. In human skin, the published literature has only confirmed scalp skin and scalp hair follicles (HFs) as cutaneous sources of extra-pituitary PRL production [1], PRL expression has been reported in human dermal fibroblasts in vitro [8]. El-Khateeb et al [5] recently reported increased levels of PRL in blister fluid from lesional psoriatic skin in psoriasis patients when compared to uninvolved skin and skin from healthy subjects. These levels exceeded serum PRL levels; evidence that PRL is produced intracutaneously. Given the pro-inflammatory cutaneous cytokine milieu which is present in psoriasis, we speculated that cytokines, for example tumour necrosis factor alpha (TNFa) and interferon gamma (IFNc), may up-regulate intracutaneous PRL production
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