A novel mechanism in control of human pigmentation by β-melanocyte-stimulating hormone and 7-tetrahydrobiopterin

Spencer, Jennifer D; Chavan, Bhaven; Marles, Lee K.; Kauser, Söbia; Rokos, Hartmut; Schallreuter, Karin U.

doi:10.1677/joe.1.06275

Cited by 34 publications

(35 citation statements)

References 40 publications

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“…6BH4 also serves as a cofactor for phenylalanine and tyrosine hydroxylase. In addition, 7BH4, an isomer of 6BH4 and an inhibitor of tyrosinase, was shown to be present in melanosomes [137]. Interestingly, only b-MSH, but not a-MSH, would remove 7BH4 inhibitory activity [137].…”

Section: Paracrine Melanogenic Stimulatorsmentioning

confidence: 99%

Cellular mechanisms regulating human melanogenesis

Park

Kosmadaki

Yaar

et al. 2009

Cell. Mol. Life Sci.

323

354

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The major differentiated function of melanocytes is the synthesis of melanin, a pigmented heteropolymer that is synthesized in specialized cellular organelles termed melanosomes. Mature melanosomes are transferred to neighboring keratinocytes and are arranged in a supranuclear cap, protecting the DNA against incident ultraviolet light (UV) irradiation. The synthesis and distribution of melanin in the epidermis involves several steps: transcription of melanogenic proteins, melanosome biogenesis, sorting of melanogenic proteins into the melanosomes, transport of melanosomes to the tips of melanocyte dendrites and finally transfer into keratinocytes. These events are tightly regulated by a variety of paracrine and autocrine factors in response to endogenous and exogenous stimuli, principally UV irradiation.

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Section: Paracrine Melanogenic Stimulatorsmentioning

confidence: 99%

Cellular mechanisms regulating human melanogenesis

Park

Kosmadaki

Yaar

et al. 2009

Cell. Mol. Life Sci.

323

354

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“…44 In general, melanogenesis is regulated by several local factors including POMC and its derivative peptides, particularly alpha-melanocyte-stimulating hormone (a-MSH); by the activity of melanocortin-1 receptor (MC1R) on melanocytes; and by cytokines and growth factors in the microenvironment. 35,45,46 These factors have the capacity to activate MITF, which in turn regulates genes encoding enzymes driving the process of melanogenesis, including tyrosinase, TYRP-1, and TYRP-2. 19 The functional activity of tyrosinase in the complex conversion of tyrosine to melanin is supported by p protein and membrane-associated transporter protein (MATP), which provide an appropriate ionic environment.…”

Section: Melanin Biosynthesis and Distributionmentioning

confidence: 99%

Melanocyte Biology and Function with Reference to Oral Melanin Hyperpigmentation in HIV-Seropositive Subjects

Feller

Chandran

Kramer

et al. 2014

AIDS Research and Human Retroviruses

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The color of normal skin and of oral mucosa is not determined by the number of melanocytes in the epithelium but rather by their melanogenic activity. Pigmented biopolymers or melanins are synthesized in melanosomes. Tyrosinase is the critical enzyme in the biosynthesis of both brown/black eumelanin and yellow/red pheomelanin. The number of the melanosomes within the melanocytes, the type of melanin within the melanosomes, and the efficacy of the transfer of melanosomes from the melanocytes to the neighboring keratinocytes all play an important role in tissue pigmentation. Melanin production is regulated by locally produced factors including proopiomelanocortin and its derivative peptides, particularly alpha-melanocyte-stimulating hormone (α-MSH), melanocortin 1 receptor (MC1R), adrenergic and cholinergic agents, growth factors, cytokines, and nitric oxide. Both eumelanin and pheomelanin can be produced by the same melanocytes, and the proportion of the two melanin types is influenced by the degree of functional activity of the α-MSH/MC1R intracellular pathway. The cause of HIV oral melanosis is not fully understood but may be associated with HIV-induced cytokine dysregulation, with the medications commonly prescribed to HIV-seropositive persons, and with adrenocortical dysfunction, which is not uncommon in HIV-seropositive subjects with AIDS. The purpose of this article is to discuss some aspects of melanocyte biology and HIV-associated oral melanin hyperpigmentation.

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“…There is much evidence that suggests constant accumulation of H 2 O 2 leading to a cascade of impaired signals in active vitiligo (7)(8)(9)(10)(11). Moreover, the calmodulin-regulated calcium homeostasis is altered by H 2 O 2 -mediated stress due to the loss of calcium binding on the protein (6).…”

Section: Introductionmentioning

confidence: 99%

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

Song

Xu²,

Pan³

et al. 2008

Int J Mol Med

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Abstract.Vitiligo is an acquired and progressive disorder manifested by the selective destruction of melanocytes in the skin. An extremely high level of hydrogen peroxide (H 2 O 2 ) in plasma as well as in lesional skin has been reported in vitiligo patients. High H 2 O 2 level has been suggested to be responsible for the disappearance of melanocytes in vitiligo. JNK and p38 MAPK are strongly induced by oxidative stress and related to neuron loss in neurodegenerative disorders. Minocycline, an antibiotic possessing antioxidant activity, is capable of attenuating oxidative stress-induced neurotoxicity. To investigate whether minocycline rescues melanocytes from H 2 O 2 -induced apoptosis, cultured mouse melanocytes (B10BR) were treated with H 2 O 2 in the presence or absence of minocycline. Our data showed that H 2 O 2 decreases cell viability in a concentration-dependent manner which is attenuated by minocycline. Also, H 2 O 2 treatment activates JNK and p38 MAPK, and executive caspase 3 in B10BR cells. Minocycline significantly inhibits H 2 O 2 -induced activation of JNK, p38 MAPK and caspase 3. Collectively, we concluded that minocycline protects melanocytes against H2O2-induced apoptosis in vitro. Its protective effect is associated with the inhibition of JNK and p38 MAPK. Our findings suggest that minocycline, a clinically well-tolerated, safe antibiotic, may be used to prevent melanocyte loss in the early stage of vitiligo.

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A novel mechanism in control of human pigmentation by β-melanocyte-stimulating hormone and 7-tetrahydrobiopterin

Cited by 34 publications

References 40 publications

Cellular mechanisms regulating human melanogenesis

Cellular mechanisms regulating human melanogenesis

Melanocyte Biology and Function with Reference to Oral Melanin Hyperpigmentation in HIV-Seropositive Subjects

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

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