Stimulation of Human Melanocytes by Vitamin D3 Possibly Mediates Skin Pigmentation After Sun Exposure

Tomita, Yasushi; Torinuki, Wakio; Tagami, Hachiro

doi:10.1111/1523-1747.ep12462151

Cited by 63 publications

(56 citation statements)

References 10 publications

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“…25) is responsible for skin darkening. However, overproduction or dysregulation of melanin pigments can cause skin hyperpigmentation disorders such as freckles, melasma, ephelides, senile lentigo, and age spots.…”

Section: Discussionmentioning

confidence: 99%

4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

Kim¹,

Lee

et al. 2005

Biological & Pharmaceutical Bulletin

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Tyrosinase (monophenol, dihydroxy-L-phenylalanin: oxygen oxidoreductase, EC 1.14.18.1) is a copper-dependent protein widely distributed in nature.2) The enzyme catalyzes two different reactions: the hydroxylation of monophenols to o-diphenols (monophenolase activity) and the oxidation of odiphenols to o-quinones (diphenolase activity), both utilizing molecular oxygen.3)The enzymatic browning of fruits and vegetables is mostly related to the oxidation of endogenous phenolic containing compounds catalyzed by polyphenol oxidase. 4) Tyrosinase also is responsible for melanization in animals, and is the key enzyme for the regulation of melanogenesis in mammals. 5)Melanin is synthesized in epidermal melanocytes, and then is transferred into epidermal keratinocytes via the melanocytes' dendrites. 6) Melanogenesis is the process by which melanin is produced (and subsequently distributed) by melanocytes within the skin and hair follicles.7) This process results in the synthesis of melanin pigments, which plays a protective role against skin photocarsinogenesis.8) The main physiological stimulus of melanogenesis is the ultraviolet radiation of solar light, which can act directly on melanocytes or indirectly through the release of keratinocyte-derived factors such as MSH (a-melanocyte stimulating hormone). 9)One of the biggest causative agents of hyperpigmentaion is probably UV light. 10) However, skin darkening can be suppressed, at least partially, by deactivating of tyrosinase. 11)Therefore, tyrosinase inhibitors have become increasingly important in the cosmetic and medicinal products used in the prevention of hyperpigmentaion.12) Many compounds, such as hydroquinone, 13) kojic acid, 14) and benzaldehyde-O-alkyloximes 15) have been reported as tyrosinase inhibitors. The established murine B16F10 melanoma cell (B16 cells) line offers a model system with readily quantifiable markers that are characteristic of differentiating, including melanogenesis. 16) In B16 cells, a-tocopheryl ferulate was shown to have depigmenting effect. 17) Although 4,4Ј-dihydroxybiphenyl (44Ј-BP), a bisphenol derivative was known as a radical scavenger for methacrylate polymerization, 18) but its efficacy on tyrosinase inhibition and melanin biosynthesis has not been reported.The aim of this study was to characterize inhibition mode of 44Ј-BP on mushroom tyrosinase. We also examined the inhibitory effect of 44Ј-BP on melanin biosynthesis, and cell viability in B16 cells as a biomarker for the potential cytotoxicity. Cell Culture B16 cells (from Korean Cell Line Bank) were cultured in DMEM with 10% fetal bovine serum (FBS; Gibco) and penicillin/streptomycin (100 IU/50 mg/ml) in a humidified atmosphere containing 5% CO 2 in air at 37°C. B16 cells were cultured in 24-well plates for the melanin quantification and enzyme activity assays. MATERIALS AND METHODS MaterialsDetermination of 44-BP for Cell Viability The cell proliferation assay was carried out by the method of Tada et al. using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (...

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Section: Discussionmentioning

confidence: 99%

4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

Kim¹,

Lee

et al. 2005

Biological & Pharmaceutical Bulletin

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“…Indeed, over a physiologic range of UV doses, NGF supple-mentation of cultured melanocytes and human melanoma cells was found to enhance cell survival and markedly reduce the characteristic DNA compaction, magination and eventual fragmentation of apoptosis (108) that was observed in the ultraviolet-irradiated pigment cells under basal culture conditions (109). Recent studies (1 10) suggest that NGF acts to prevent ultraviolet-induced melanocyte cell death by upregulating the anti-apoptotic bcl-2 gene ( 1 1 1-1 13) that, interestingly, is reported to be strongly expressed by melanocytes in viva even in the absence of ultraviolet irradiation ( 1 14). Thus, considerable data suggest a role in the tanning response for NGF, acting through ~7 .…”

Section: Role Of Neurotrophinsmentioning

confidence: 99%

Mechanisms of Ultraviolet Light‐Induced Pigmentation

Gilchrest

Park

Eller

et al. 1996

Photochem & Photobiology

322

231

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“…isobutylmethylxanthine) can stimulate melanogenesis (6). Additionally, the protein kinase C (PKC) 1 pathway was thought to be involved in the regulation of melanogenesis. Indeed, 1-oleyl-2-acetyl-glycerol, a PKC activator, stimulates melanogenesis (9,10,15), and a direct correlation between the level of PKC activity in melanocytes and the activity of tyrosinase has been shown (16).…”

mentioning

confidence: 99%

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

Romero-Graillet

Aberdam

Biagoli

et al. 1996

Journal of Biological Chemistry

168

144

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Ultraviolet B (UVB) radiation is the main physiological stimulus for human skin pigmentation; however, the molecular mechanisms underlying this process are still unclear. Recently, nitric oxide (NO) and cGMP have been involved in mediation of skin erythema induced by UVB. Therefore, we investigated the role of NO and cGMP in UVB-induced melanogenesis. In this study, we demonstrated that UVB stimulation of melanogenesis was mimicked by exogenous NO donors. Additionally, we showed that NO stimulated cGMP synthesis and that cGMP was also a potent stimulator of melanogenesis. Furthermore, the inhibition of the melanogenic effect of NO by guanylate cyclase inhibitor demonstrated that NO mediated its effect through the activation of guanylyl cyclase. Interestingly, 1 min after UVB irradiation, we observed a significant increase in cGMP content in melanocytes. The effects of UVB on cGMP production and on melanogenesis were blocked by both guanylate cyclase and NO synthase inhibitors. Additionally, inhibition of cGMP-dependent kinase also prevented the stimulation of melanogenesis by UVB and NO. Therefore, we concluded that NO and cGMP production is required for UVB-induced melanogenesis and that cGMP mediated its melanogenic effects mainly through the activation of cGMP-dependent kinase.Epidermal melanin is responsible for skin darkening and is synthesized by melanocytes as the result of a cascade of enzymatic reactions. Tyrosinase, which converts tyrosine to dopaquinone, is the rate-limiting enzyme involved in melanin synthesis and represents the major regulatory step in melanogenesis. Numerous stimuli are able to alter melanogenesis of cultured pigmented cells; vitamin D metabolites (1), retinoids (2, 3), melanocyte-stimulating hormone (4 -6), forskolin, cholera toxin, isobutylmethylxanthine (7,8), diacylglycerol analogs (9, 10), and UV irradiation (11)(12)(13)(14). Until now the molecular mechanism involved in the induction of melanogenesis by these agents was not fully elucidated. A role for the cAMP pathway has been proposed on the basis that adenylate cyclase activators such as melanocyte-stimulating hormone, forskolin, and cholera toxin or phosphodiesterase inhibitors (e.g. isobutylmethylxanthine) can stimulate melanogenesis (6). Additionally, the protein kinase C (PKC) 1 pathway was thought to be involved in the regulation of melanogenesis. Indeed, 1-oleyl-2-acetyl-glycerol, a PKC activator, stimulates melanogenesis (9, 10, 15), and a direct correlation between the level of PKC activity in melanocytes and the activity of tyrosinase has been shown (16). However, induction of melanogenesis by UVB or by 1-oleyl-2-acetyl-glycerol is unaffected by RO 31-8220, a PKC inhibitor (17), leading to the conclusion that protein kinase C does not play a pivotal role in the control of melanogenesis. In humans, only UVB radiation represents an established physiological stimulus of melanogenesis, and despite many efforts to identify the molecular events triggered by UVB radiation, the mechanisms underlying UVB-induced melanogene...

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Stimulation of Human Melanocytes by Vitamin D3 Possibly Mediates Skin Pigmentation After Sun Exposure

Cited by 63 publications

References 10 publications

4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

Mechanisms of Ultraviolet Light‐Induced Pigmentation

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

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Stimulation of Human Melanocytes by Vitamin D3 Possibly Mediates Skin Pigmentation After Sun Exposure

Cited by 63 publications

References 10 publications

4,4&prime;-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

4,4&prime;-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

Mechanisms of Ultraviolet Light‐Induced Pigmentation

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

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4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor

4,4′-Dihydroxybiphenyl as a New Potent Tyrosinase Inhibitor