Abstract
The melanocortin system is a major regulator of stress responses in the skin and is responsible for the induction of melanin synthesis through activation of melanogenesis enzymes. The expression of both melanocortin system genes and melanogenesis enzyme genes is altered in psoriasis, and the focus here was on twelve genes related to the signal transduction between them. Additionally, five endogenous opioid system genes that are involved in cutaneous inflammation were examined. Quantitative real-time-PCR was utilized to measure mRNA expression in punch biopsies from lesional and non-lesional skin of psoriasis patients and from the skin of healthy control subjects. Most of the genes related to melanogenesis were down-regulated in patients (CREB1, MITF, LEF1, USF1, MAPK14, ICAM1, PIK3CB, RPS6KB1, KIT, and ATRN). Conversely, an up-regulation occurred in the case of opioids (PENK, PDYN, and PNOC). The suppression of genes related to melanogenesis is in agreement with the reported reduction in pigmentation signaling in psoriatic skin and potentially results from the pro-inflammatory environment. The increase in endogenous opioids can be associated with their involvement in inflammatory dysregulation in psoriasis.
Highlights
Psoriasis is a chronic, relapsing, inflammatory skin disease that generally affects around 2–4% of the population in Western countries [1,2]
The melanocortin system has been identified among these numerous intertwined networks, with proopiomelanocortin (POMC) as its central molecule. It is a highly hierarchical network composed of α, β, and γ-melanocyte-stimulating hormone (MSH) and adrenocorticotropin (ACTH), all four of which are derived from POMC, five melanocortin receptors (MCR1-5), and two melanocortin receptor antagonists: agouti signaling protein (ASIP) and agouti-related protein (AGRP)
The genes associated with the intracellular signaling system linking melanocortin receptors with enzymes involved in melanin synthesis were generally suppressed in psoriasis
Summary
Psoriasis is a chronic, relapsing, inflammatory skin disease that generally affects around 2–4% of the population in Western countries [1,2]. We showed significant alterations in the expression of genes of the melanocortin system in the skin of psoriasis patients [16]. The system of endogenous opioids in the skin includes several neuromediators, which derive from four different precursors, namely, POMC, proenkephalin (PENK), prodynorphin (PDYN), and prepronociceptin (PNOC), and their receptors [18,19]. Considering our former findings describing the altered expression of melanocortin genes and melanogenesis enzymes in psoriasis, aberrations could be suspected in the factors involved in signal transduction between them. Main known reg light gray and the associated factors that were investigated in this study are indicated with da of melanogenesis. 1. Main known regulatory links genes of the melanocortin system and enzymes in lesional psoriasis skin. The up-regulation of PENK was detected in lesional skin compared to non-lesional psoriasis skin
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