Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Scott, Glynis; Fricke, Alex F.; Fender, Anne; McClelland, Lindy; Jacobs, Stacey E.

doi:10.1016/j.yexcr.2007.07.039

Cited by 27 publications

(28 citation statements)

References 61 publications

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“…[33][34][35][36] We then measured PGE 2 release from cultured keratinocytes treated by squalene peroxide. Keratinocytes were treated by squalene peroxide mixture (12.5-50 mM) for 24 h. Squalene peroxide dramatically increased PGE 2 release from keratinocytes in a dose-dependent manner (Fig.…”

Section: Effect Of Squalene Peroxide On Melanin Synthesis Of Culturedmentioning

confidence: 99%

Squalene as a Target Molecule in Skin Hyperpigmentation Caused by Singlet Oxygen

Ryu

Arakane

Koide

et al. 2009

Biological & Pharmaceutical Bulletin

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It has been postulated that reactive oxygen species generated by UV irradiation contribute to photo-induced skin damage, such as lipid peroxidation, sunburn reaction, phototoxicity, photoallergy, and photo-aging. [1][2][3][4][5][6][7][8] However, the mechanistic details remain unclear. Among various reactive oxygen species, singlet oxygen, a highly reactive and toxic intermediate with specific reactivity, appears to play an important role because it mediates photosensitized reactions. 9,10) We previously constructed a very sensitive near-infrared emission spectrometer with a germanium (Ge)-detector as a reliable means of singlet oxygen detection. [11][12][13] We used this device to show that coproporphyrin from Propionibacterium acnes (P. acnes) generated singlet oxygen on the surface of healthy skin under UV exposure by detecting the emission at 1268 nm due to singlet oxygen. 13) Patients with erythropoietic protoporphyria, caused by accumulation of protoporphyrin in the skin, are known to suffer severe skin damage during sunlight exposure.14,15) Our data suggested that damage might also occur in healthy skin. In addition, UVA-induced singlet oxygen generation has been shown to induce lipid peroxidation and gene expression. [16][17][18][19] Minami et al. reported that singlet oxygen was involved in UVA-induced oxidation of oleic acid and linoleic acid in mouse skin. However, singlet oxygen generated from coproporphyrin on the human skin surface should immediately attack skin surface lipids, which are mainly derived from sebaceous gland lipids such as triacylglycerol, free fatty acid, wax, squalene and cholesterol. 16,20) Because squalene was hardly oxidized in vitro under UV irradiation alone, a contribution of a factor producing singlet oxygen to squalene peroxidation in the skin was suggested. 21) Thus, there have been several investigations of singlet oxygen and endogenous photosensitizers in the skin under physiological conditions. [22][23][24] Lipid peroxide induces further reactions and is associated with the pathology of acne, atopic dermatitis, psoriasis and pigmentation. 25,26) However, the precise involvement of lipid peroxide in these pathologies has not been well investigated.Here, we first examined the reactivity of squalene with singlet oxygen directly by detection of singlet oxygen emission at 1268 nm and clarified the contribution of coproporphyrin as a photosensitizer to squalene peroxide formation under UV exposure. Then we demonstrated that squalene peroxide participates in UVA-induced skin hyperpigmentation. Cell Culture Human epidermal melanocytes were cultured in the MEDIUM 254 supplemented with the human melanocyte growth supplement (HMGS) at 37°C in 5% CO 2 /95% air condition. Human epidermal keratinocytes were cultured in the HuMedia-KG2 with 0.03 mM CaCl 2 , and hydrocortisone was removed from media 72 h before treatments. Cells and media were from Kurabo Industries Ltd. (Osaka, Japan). MATERIALS AND METHODS MaterialsAnimals Five-week-old female A-1 strain brownish guinea pigs were pur...

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Section: Effect Of Squalene Peroxide On Melanin Synthesis Of Culturedmentioning

confidence: 99%

Squalene as a Target Molecule in Skin Hyperpigmentation Caused by Singlet Oxygen

Ryu

Arakane

Koide

et al. 2009

Biological & Pharmaceutical Bulletin

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“…However, PGE 2 has a direct effect on melanocyte-mediated post-inflammatory pigmentary responses and melanocyte dendricity showing relevance to skin tanning [27,38].…”

Section: Cyclooxygenase-derived Mediatorsmentioning

confidence: 99%

“…PGF 2α has been found in whole skin and keratinocytes in culture [21,22,47] and has been linked to inflammation, immune responses, pigmentation and hair growth [27,38,48]. The effects of PGF 2α are mediated through the FP receptor found expressed in epidermal cells and melanocytes [49][50][51].…”

Section: Cyclooxygenase-derived Mediatorsmentioning

confidence: 99%

Eicosanoids in skin inflammation

Nicolaou

2013

Prostaglandins, Leukotrienes and Essential Fatty Acids

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SummaryEicosanoids play an integral part in homeostatic mechanisms related to skin health and structural integrity. They also mediate inflammatory events developed in response to environmental factors, such as exposure to ultraviolet radiation, and inflammatory and allergic disorders, including psoriasis and atopic dermatitis. This review article discusses biochemical aspects related to cutaneous eicosanoid metabolism, the contribution of these potent autacoids to skin inflammation and related conditions, and considers the importance of nutritional supplementation with bioactives such as omega-3 and omega-6 polyunsaturated fatty acids and plant-derived antioxidants as means of addressing skin health issues.2

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“…5 In addition, prostaglandins (PGs) are key mediators of diverse functions in the skin; and several reports 6,7 have suggested that PGs mediate postinflammatory pigmentary changes by modulating melanin synthesis and melanocyte dendricity.…”

mentioning

confidence: 99%

“…[2][3][4] The two main paracrine melanogenic cytokines, stem cell factor (SCF) and endothelin (ET)-1, have been demonstrated to play pivotal roles in skin pigmentation, including UV-Binduced pigmentation. 5 In addition, prostaglandins (PGs) are key mediators of diverse functions in the skin; and several reports 6,7 have suggested that PGs mediate postinflammatory pigmentary changes by modulating melanin synthesis and melanocyte dendricity.…”

mentioning

confidence: 99%

UV-B Radiation Induces Macrophage Migration Inhibitory Factor–Mediated Melanogenesis through Activation of Protease-Activated Receptor-2 and Stem Cell Factor in Keratinocytes

Enomoto

Yoshihisa

Yamakoshi

et al. 2011

The American Journal of Pathology

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UV radiation indirectly regulates melanogenesis in melanocytes through a paracrine regulatory mechanism involving keratinocytes. Protease-activated receptor (PAR)-2 activation induces melanosome transfer by increasing phagocytosis of melanosomes by keratinocytes. This study demonstrated that macrophage migration inhibitory factor (MIF) stimulated PAR-2 expression in human keratinocytes. In addition, we showed that MIF stimulated stem cell factor (SCF) release in keratinocytes; however, MIF had no effect on the release of endothelin-1 or prostaglandin E2 in keratinocytes. In addition, MIF had no direct effect on melanin and tyrosinase synthesis in cultured human melanocytes. The effect of MIF on melanogenesis was also examined using a three-dimensional reconstituted human epidermal culture model, which is a novel, commercially available, cultured human epidermis containing functional melanocytes. Migration inhibitory factor induced an increase in melanin content in the epidermis after a 9-day culture period. Moreover, melanin synthesis induced by UV-B stimulation was significantly down-regulated by anti-MIF antibody treatment. An in vivo study showed that the back skin of MIF transgenic mice had a higher melanin content than that of wild-type mice after 12 weeks of UV-B exposure. Therefore, MIFmediated melanogenesis occurs mainly through the activation of PAR-2 and SCF expression in keratino- Exposure to UV radiation leads to various short-term deleterious cutaneous effects, including sunburn and immunosuppression, and long-term consequences that lead to premature aging, including hyperpigmentation.1 UV radiation indirectly regulates melanogenesis in melanocytes through a paracrine regulatory mechanism involving keratinocytes. UV-B-induced pigmentation occurs when human keratinocytes exposed to UV-B are stimulated to produce and secrete several mediators that trigger the activation of melanocytes and act as potent mitogens and melanogens for human melanocytes.2-4 The two main paracrine melanogenic cytokines, stem cell factor (SCF) and endothelin (ET)-1, have been demonstrated to play pivotal roles in skin pigmentation, including UV-Binduced pigmentation. 5 In addition, prostaglandins (PGs) are key mediators of diverse functions in the skin; and several reports 6,7 have suggested that PGs mediate postinflammatory pigmentary changes by modulating melanin synthesis and melanocyte dendricity.Protease-activated receptor (PAR)-2 is a member of a novel G-protein-coupled seven-transmembrane receptor family.8 These receptors are irreversibly activated through proteolytic cleavage of their amino termini. Subsequent to proteolytic cleavage, the newly exposed NH2 terminus acts as a tethered peptide ligand, which binds and activates the receptor. Protease-activated receptor-2 is involved in skin pigmentation because it increases the phagocytosis of melanosomes by keratinocytes.9 UV ir-

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Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Cited by 27 publications

References 61 publications

Squalene as a Target Molecule in Skin Hyperpigmentation Caused by Singlet Oxygen

Squalene as a Target Molecule in Skin Hyperpigmentation Caused by Singlet Oxygen

Eicosanoids in skin inflammation

UV-B Radiation Induces Macrophage Migration Inhibitory Factor–Mediated Melanogenesis through Activation of Protease-Activated Receptor-2 and Stem Cell Factor in Keratinocytes

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