Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.10.3.1 (tyrosinase)
9,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Compelling evidence suggest a role for melanocortins in the regulation of melanogenesis by ultraviolet radiation. Within the epidermis, melanocytes and keratinocytes produce alpha-melanocyte-stimulating hormone and adrenocorticotropic hormone. The persistence and the strength of the biologic signal delivered by these peptides depend on their local concentration, which is controlled by the rate of peptide production and by the rate of its degradation. In this study, we investigated the mechanism of melanocortin degradation by melanocytes and the effect of ultraviolet on this process. We have focused our attention on a neutral endopeptidase, neprilysin, which has been implicated in the ending of numerous peptidergic signals. We have shown that this enzyme is expressed at the surface of human melanocytes. Interestingly, its activity and its expression are dramatically downregulated by ultraviolet B treatment. Moreover, in the presence of phosphoramidon, a stable inhibitor of neprilysin, we observed an increased efficiency of alpha-melanocyte-stimulating hormone and adrenocorticotropic hormone to stimulate both tyrosinase activity and microphthalmia expression. Taken together, these data indicate that neprilysin expressed by melanocytes has a physiologic role in the regulation of melanogenesis by proopiomelanocortin peptide. Further, its downregulation by ultraviolet B irradiation shed light on a new and appealing mechanism of ultraviolet B induced melanogenesis via the control of melanocortins degradation.
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PMID:Neprilysin, a novel target for ultraviolet B regulation of melanogenesis via melanocortins. 1095 Dec 72

Exposure of human skin to ultraviolet (UV) radiation causes significant damage to that tissue. The effects of UV on the skin mainly include acute inflammation (erythema/edema) and abnormal keratinization wherein prostaglandin E2 (produced by cyclooxygenase-2), interleukin-8 and transglutaminase 1 (a major regulatory factor of keratinization) play pivotal roles. Later phases of UV-induced skin reactions include hyperpigmentation, wrinkle formation and carcinogenesis, the former two being associated with the UVB-induced production and/or secretion of endothelin-1, stem cell factor and granulocyte-macrophage colony-stimulating factor by keratinocytes in the epidermis. Those paracrine factors then stimulate expression of the critical melanogenic enzyme tyrosinase by melanocytes in the epidermis and increase expression of neprilysin, an enzyme that degrades elastin, by fibroblasts in the dermis. This review summarizes the biological effects of the xanthophyll carotenoid astaxanthin, which prevents UV-induced cutaneous inflammation, abnormal keratinization and wrinkling as well as pigmentation of the skin even by its postirradiation treatment.
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PMID:The Xanthophyll Carotenoid Astaxanthin has Distinct Biological Effects to Prevent the Photoaging of the Skin Even by its Postirradiation Treatment. 3033 60