Physiological factors that regulate skin pigmentation

Yamaguchi, Yuji; Hearing, Vincent J.

doi:10.1002/biof.29

Cited by 418 publications

(439 citation statements)

References 58 publications

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“…Melanogenesis has been the interest of intense research for many decades. Melanocytes are unique cells that produce melanosomes, specific melanin-containing intracellular organelles [45]. In our study, the effect of lomefloxacin on melanocytes viability was analyzed.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic effect of lomefloxacin in culture of human epidermal melanocytes

Beberok

Otręba

Wrześniok

et al. 2013

Pharmacological Reports

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Abstract:Backround: Lomefloxacin is a potent bactericidal antibiotic. The use of this drug in treatment of various infections is accompanied by serious adverse effects on pigmented tissues. The exact mechanisms of lomefloxacin side effects have not been well established yet. The aim of this study was to characterize the interaction between lomefloxacin and melanin, and to examine how this interaction affects the cell viability and melanization in melanocytes. Methods: Normal human epidermal melanocytes and the model DOPA-melanin were used. The binding parameters of lomefloxacin-melanin complexes as well as the antibiotic effect on cell viability and melanization in pigmented cells were investigated using a spectrophotometric method. Results: Our results indicate that lomefloxacin forms stable complexes with melanin. The analysis of drug binding to melanin has shown that at least two classes of independent binding sites are involved in formation of these complexes. The WST-1 assay was used to detect the antibiotic cytotoxic effect. The value of ED 50 for lomefloxacin was about 0.75 mmol/l. It has been shown that lomefloxacin causes inhibition of tyrosinase activity, and reduces melanin content in human skin melanocytes in a dose-dependent manner. Conclusion:The ability of the analyzed fluoroquinolone to form complexes with melanin, and the demonstrated inhibitory effect on a melanization process in melanocytes in vitro may explain a potential role of melanin biopolymer in the mechanisms of undesirable side effects of lomefloxacin in vivo resulting from its accumulation in pigmented tissues.

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Section: Discussionmentioning

confidence: 99%

Cytotoxic effect of lomefloxacin in culture of human epidermal melanocytes

Beberok

Otręba

Wrześniok

et al. 2013

Pharmacological Reports

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“…We found that gd TCR + intraepithelial lymphocytes were reduced by 50% in AhR-KO mice, but frequencies of gd T cells in blood or spleen did not differ between AhR genotypes (Supplemental Data 3D, 3E). It is known that the ligand of c-Kit, stem cell factor (SCF), is secreted by epidermal cells (38). We therefore hypothesized that SCF/c-Kit signaling might be affected by AhR deficiency.…”

Section: C-kit Expression Is Ahr Dependentmentioning

confidence: 99%

Aryl Hydrocarbon Receptor Is Critical for Homeostasis of Invariant γδ T Cells in the Murine Epidermis

Kadow

Jux

Zahner

et al. 2011

The Journal of Immunology

133

123

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An immunoregulatory role of aryl hydrocarbon receptor (AhR) has been shown in conventional αβ and γδ T cells, but its function in skin γδ T cells (dendritic epidermal T cells [DETC]) is unknown. In this study, we demonstrate that DETC express AhR in wild-type mice, and are specifically absent in the epidermis of AhR-deficient mice (AhR-KO). We show that DETC precursors are generated in the thymus and home to the skin. Proliferation of DETC in the skin was impaired in AhR-KO mice, resulting in a >90% loss compared with wild type. Surprisingly, DETC were not replaced by αβ T cells or conventional γδ T cells, suggesting a limited time frame for seeding this niche. We found that DETC from AhR-KO mice failed to express the receptor tyrosine kinase c-Kit, a known growth factor for γδ T cells in the gut. Moreover, we found that c-kit is a direct target of AhR, and propose that AhR-dependent c-Kit expression is potentially involved in DETC homeostasis. DETC are a major source of GM-CSF in the skin. Recently, we had shown that impaired Langerhans cell maturation in AhR-KO is related to low GM-CSF levels. Our findings suggest that the DETCs are necessary for LC maturation, and provide insights into a novel role for AhR in the maintenance of skin-specific γδ T cells, and its consequences for the skin immune network.

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“…It has been reported that skin pigmentation is regulated by a variety of intrinsic and extrinsic factors [7,8] , as well as diverse signaling pathways including protein kinase A (PKA), phosphatidylinositol 3-kinase (PI3K), and mitogen-activated protein kinases (MAPKs) [9][10][11][12][13] . In particular, the MAPK kinase (MEK)/extracellular signal-regulated kinase (ERK) and the PI3K/Akt pathways have been shown to negatively regulate melanin synthesis in melanocytes and melanoma cells [14][15][16][17][18] .…”

Section: Introductionmentioning

confidence: 99%

[6]-Shogaol inhibits melanogenesis in B16 mouse melanoma cells through activation of the ERK pathway

Cheng

et al. 2012

Acta Pharmacol Sin

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Aim:To investigate the effect of [6]-shogaol, an active ingredient in ginger, on melanogenesis and the underlying mechanisms. Methods: B16F10 mouse melanoma cells were tested. Cell viability was determined with the MTT assay. Melanin content and tyrosinase activity were analyzed with a spectrophotometer. The protein expression of tyrosinase and microphthalmia associated transcription factor (MITF), as well as phosphorylated or total ERK1/2 and Akt were measured using Western blot.

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Physiological factors that regulate skin pigmentation

Cited by 418 publications

References 58 publications

Cytotoxic effect of lomefloxacin in culture of human epidermal melanocytes

Cytotoxic effect of lomefloxacin in culture of human epidermal melanocytes

Aryl Hydrocarbon Receptor Is Critical for Homeostasis of Invariant γδ T Cells in the Murine Epidermis

[6]-Shogaol inhibits melanogenesis in B16 mouse melanoma cells through activation of the ERK pathway

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