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Melanin Production (melanin + production)
Selected AbstractsCell Shape Normalization, Dendrite Orientation, and Melanin Production of Normal and Genetically Altered (Haploinsufficient NF1)-Melanocytes by Microstructured Substrate InteractionsCHEMPHYSCHEM, Issue 1 2004Simon Jungbauer Abstract Little is known about how functional regulation failure in genetically altered cells is influenced by topographical confinement of cells, a situation often present in tissues in vivo. We used cultured melanocytes derived from human skin samples as a model system for such investigations. Normal melanocytes have a very well defined shape consisting of a cell body and two dendrites arranged 180° relative to each other. In contrast, neurofibromin 1-melanocytes (NF1-melanocytes) have up to a 50,% reduction of neurofibromin 1, which results in an altered morphology that can be easily measured. NF1-melanocytes deviate from the defined structure of normal melanocytes by forming more than two dendrites per cell. We show that morphology consequences of genetically altered melanocytes can be canceled if cells interact with substrates microstructured by stripes that apply mechanophysical signals in the form of physical topography. The strength of the mechanophysical signal was varied systematically by increasing the height of the microstructures. Melanocytes respond to surface topographical features that are larger than 50 nm and have lateral confinements smaller 4 ,m. The response of normal and NF1-melanocytes to different topographies was analyzed quantitatively by determining density distributions for the number of dendrites per cell, the angles between dendrites, and the orientation imprinted in the substrate. The synthesis of melanin, a pigment produced by melanocytes, differs in the case of genetically altered NF1- and normal melanocytes. In both cases, the interaction with microstripes enhanced melanin production significantly. This enhanced melanin production is speculated to be caused by the mechanical stabilization of the dendrites by substrate guidance. [source] Molecular cloning of two prophenoloxidase genes from the mosquito Aedes aegyptiINSECT MOLECULAR BIOLOGY, Issue 1 2001A. S. Taft Abstract The biosynthesis of melanotic materials is an important process in the life of a mosquito. Melanin production is critical for many diverse processes such as egg chorion tanning, cuticular sclerotization, and melanotic encapsulation of metazoan parasites. Prophenoloxidase plays a critical role in this biochemical cascade. Two cDNAs, one full length and one partial clone, and two genomic clones encoding prophenoloxidase (pro-PO) were isolated from the yellow fever mosquito, Aedes aegypti. The full-length cDNA, pAaProPO1, is 2286 bp long with a 2055 bp open reading frame encoding a 685 amino acid protein that shares 89% identity with Armigeres subalbatus pro - PO. It contains two putative copper binding domains (amino acids 197,243 and 346,423) that are homologous to other insect pro-POs. AaProPO1 messenger RNA (mRNA) was detected by reverse transcription polymerase chain reaction (RT-PCR) only from third-stage larvae and not in adult mosquitoes after blood feeding, during the melanotic encapsulation of Dirofilaria immitis microfilariae or following exposure to bacteria. A 750 bp fragment of the second cDNA (pAaProPO2) was cloned using RT-PCR from mRNA obtained from 14-day postovipostional eggs. AaProPO2 mRNA was not found in any other life stages, and may be in low abundance or transiently expressed. AaProPO2 and AaProPO1 each contain three introns that are 60, 68 and 58 bp and 61, 69 and 59 bp long, respectively, and the intron sequences of these two genes are not similar. [source] Combined Excimer Laser and Topical Tacrolimus for the Treatment of Vitiligo: A Pilot StudyDERMATOLOGIC SURGERY, Issue 2 2004Adam Z. Kawalek BA Background. Vitiligo is an acquired skin disorder that is characterized by well-defined, often symmetric white patches. Although current therapeutic modalities are directed toward increasing melanocyte melanin production, few treatment modalities address the immunologic nature of the disease. Objective. To determine whether excimer laser, a known therapeutic modality, in combination with tacrolimus, a topical immunomodulator, accelerate response time and/or improve the degree of response in patients with this disorder. Methods. Eight subjects diagnosed with vitiligo were recruited to participate in this institutional review board,approved double-blind, placebo-controlled study. Twenty-four symmetric vitiliginous patches (elbows, knees) from eight subjects received excimer laser treatment three times per week for 24 treatments or 10 weeks. Additionally, topical tacrolimus 0.1% ointment (Protopic) and placebo (Aquaphor) were applied to randomized patches (left or right) twice daily throughout the length of the trial. Vitiliginous patches were monitored with photographs at baseline, every 2 weeks, and 6 months after treatment. Biopsies were performed on subjects with significant results. Results. Twenty vitiliginous patches from six subjects qualified for evaluation. Fifty percent of patches treated with combination excimer laser and tacrolimus achieved a successful response (75% repigmentation) compared with 20% for the placebo group. Subjects who responded successfully repigmented faster (19%) with combination therapy compared with excimer laser alone. Additionally, three subjects experienced transient hyperpigmentation in lesions treated with combination therapy. Conclusion. Combining topical immunomodulators with known phototherapeutic modalities may represent a key advancement in the treatment of disease. [source] Prostaglandin D2 production in FM55 melanoma cells is regulated by ,-melanocyte-stimulating hormone and is not related to melanin productionEXPERIMENTAL DERMATOLOGY, Issue 8 2010Mojgan Masoodi Please cite this paper as: Prostaglandin D2 production in FM55 melanoma cells is regulated by ,-melanocyte-stimulating hormone and is not related to melanin production. Experimental Dermatology 2010; 19: 751,753. Abstract:, This study shows that prostaglandins in human FM55 melanoma cells and epidermal melanocytes are produced by COX-1. Prostaglandin production in FM55 melanoma cells was unrelated to that of melanin suggesting that the two processes can occur independently. ,-Melanocyte-stimulating hormone, which had no effect on melanin production in FM55 cells, stimulated PGD2 production in these cells without affecting PGE2. While cAMP pathways may be involved in regulating PGD2 production, our results suggest that ,-MSH acts independently of cAMP, possibly by regulating the activity of lipocalin-type PGD synthase. This ,-MSH-mediated effect may be associated with its role as an immune modulator. [source] Why do melanomas get so dark?EXPERIMENTAL DERMATOLOGY, Issue 11 2009Rossitza Lazova Abstract:, Cutaneous malignant melanomas often exhibit pigmented regions that are darker than the surrounding skin. While melanoma cells are the original source of the melanin, keratinocytes and melanophages also contribute to the tumor colour because they contain melanin obtained from melanoma cells. However, little is known of the origin of darkly pigmented melanoma cells or of the molecular pathways regulating their melanin production. Here we discuss observations that dark melanoma cells emerge from within populations of melanoma in situ and that, in addition to producing abundant dark pigment, they appear to be undergoing autophagy. Moreover, autophagy appears to be a common trait of invasive melanoma cells in the dermis. The underlying cause of this phenomenon may stem from aberrant production of glycosylation structures known as ,1,6-branched oligosaccharides. Our studies of dark cutaneous melanomas were prompted by analyses of experimental mouse macrophage-melanoma hybrids fused in the laboratory. Like melanoma cells in cutaneous malignant melanoma, experimental hybrids also displayed abundant dark pigment and autophagy, and had high levels of ,1,6-branched oligosaccharides. Whether or not darkly pigmented malignant melanoma cells originate from fusion with macrophages in vivo remains to be determined. In any event, pigmentation in melanoma, long considered as a secondary aspect of the malignancy, may be a visible warning that the cells have gained competence for invasion and metastasis. [source] A keratinocytes,melanocytes coculture system for the evaluation of active ingredients' effects on UV-induced melanogenesisINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 1-2 2003J.-F. Nicolaÿ Synopsis A new experimental design, more reliable for in vitro testing of active ingredients' effect on ultraviolet (UV)-induced melanogenesis has been carried out. It uses a bicompartmental coculture system where cell communication between keratinocytes and melanocytes can take place. Thus, this experimental situation enables to monitor the effect of biological agents released by both cell types on melanogenesis and the interference of tested compounds with this ,paracrine linkage'. Experiments with UVB-irradiated cocultures show the importance of cell communication in the melanogenic response. In this model, the endogenous mediator, nitric oxide (NO), increased melanin production. Different compounds were tested in the coculture system, and comparison with data obtained from irradiated monocultures of melanocytes enables to distinguish a specific effect on cell communication. In addition, this more close-to-reality experimental model proved to provide a valuable first approach for the assessment of the ,bioavailability' of the tested substances. Finally, the effect of an innovative photoprotective agent capable of ,boosting' UV-induced melanogenic cell communication is presented. Résumé Un nouveau concept expérimental, plus fiable pour l,évaluation in vitro de l,effet de principes actifs sur la mélanogénèse induite par les UV, a été mis en ,uvre. Il utilise un système de co-culture à double compartiment dans lequel une communication cellulaire entre les kératinocytes et les mélanocytes peut s,établir. Ainsi, ce système expérimental permet de suivre l,effet des agents biologiques libérés par les deux types de cellules sur la mélanogénèse, et les interférences des composés testés avec ce ,lien paracrine'. Les essais avec des co-cultures irradiées aux UV montrent l,importance de la communication cellulaire dans la réponse mélanogénique. Avec ce modèle, le médiateur oxyde nitrique endogène (NO) augmente la production de mélanine. Différents composés ont été testés avec ce système de co-culture, et une comparaison avec les données obtenues à partir de monocultutres de mélanocytes irradiées permet de distinguer un effet spécifique sur la communication cellulaire. En outre, ce modèle expérimental plus proche de la réalité s,est avéré apporter une première approche valable de l,évaluation de la ,biodisponibilité' des substances testées. Enfin, l,effet d,un agent protecteur innovant capable de stimuler la communication cellulaire mélanogénique induite par les UV est décrit. [source] Inhibitory effects of 5-chloroacetyl-2-piperidino-1,3-selenazole, a novel selenium-containing compound, on skin melanin biosynthesisJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 3 2010Eunjoo H. Lee Abstract Objectives Increased production and accumulation of melanin leads to many hyperpigmentation disorders such as melasma, freckles and geriatric pigment spots. Thus, there is a need for the development of depigmenting agents. Based on our previous reports, selenium derivatives as anti-melanogenic lead compounds could be very important. The aim of this study was to investigate the depigmenting effect of novel selenium-containing compounds. Methods The inhibitory effects of 5-chloroacetyl-2-piperidino-1,3-selenazole (CS1), a novel selenium-containing compound, on melanogenesis were investigated in B16F10 melanoma cells and cultured brownish guinea pig skin tissue with ,-melanocyte-stimulating hormone stimulation. Key findings We found that CS1 inhibited melanin production in B16F10 cells by suppressing tyrosinase activity and its protein expression. In addition, Western blotting analysis revealed that CS1 suppressed the expression of tyrosinase-related protein (TRP)-1 and TRP-2. Therefore, the depigmenting effect of CS1 might have been due to inhibition of tyrosinase activity and expression of melanogenic enzymes. Furthermore, CS1 had inhibitory effects on melanin biosynthesis of primary cultured skin of brownish guinea pig. Conclusions The results suggested that CS1 could be a useful candidate for the treatment of skin hyperpigmentation. [source] Acetoside inhibits ,-MSH-induced melanin production in B16 melanoma cells by inactivation of adenyl cyclaseJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2009Ho Sun Song Abstract Objectives The aim of the study was to determine the mechanism of the whitening effect of acteoside. Methods We used tyrosinase activity and melanin production stimulated in B16 melanoma cells by ,-melanocyte stimulating hormone (,-MSH) or forskolin to measure the whitening effect of acteoside. Key findings Acteoside did not directly inhibit mushroom tyrosinase activity, but dose-dependently inhibited tyrosinase activity and melanin production in B16 melanoma cells stimulated by 1 ,mol/l ,-MSH. Acteoside also reduced cyclic AMP levels in cells stimulated by 1 ,mol/l ,-MSH, suggesting direct inhibition of adenyl cyclase. Acteoside also inhibited productionofbothmelanin and cyclic AMP in cells stimulated by 1 ,mol/l forskolin, an adenyl cyclase activator. Acteoside showed antioxidant activity in a cell-free DPPH (1-diphenyl-2-picrylhydroazyl) assay and inhibited generation of intracellular reactive oxygen species. Conclusions These results suggest that the whitening activity of acteoside results from inhibition of adenyl cyclase and ,-MSH signalling. [source] Clinical Resolution of a Neonatally Eroded Giant Congenital Melanocytic NevusPEDIATRIC DERMATOLOGY, Issue 6 2006Julia K. Gass M.R.C.P.C.H. This process has been documented with photographs and skin biopsy specimens. Neonatal histology demonstrated connective tissue proliferation. Histology at age 5 years also demonstrated a very high proportion of amelanotic dermal nevus cells. Regression of pigmentation in our patient may be due to a decrease in melanin production by dermal nevus cells rather than a decrease in their number. [source] Molecular structure and concentration of melanin in the stratum corneum of patients with melasmaPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 3 2009Benjamin Moncada Melasma is an abnormal acquired hyperpigmentation of the face of unknown origin, it is considered a single disease and very little has been found regarding its pathogenesis. It is usually assumed that melasma is due to excessive melanin production, but excessive retention or abnormal metabolism of this molecule has not yet been considered. In order to search for an alternate explanation for the excessive pigmentation in melasma the molecular structure and concentration of melanin in the stratum corneum of patients with melasma was analyzed using Raman spectroscopy and optical transmission spectroscopy, respectively. From this study it became apparent that in melasma melanin is concentrated in the deeper layers of the skin but its exteriorization remains the same as for healthy skin. Raman spectroscopy measurements showed degraded molecules of melanin in some subjects, which may help explain the variable success rate of the standard therapy. [source] Melanin biosynthesis by Frankia strain CeI5PHYSIOLOGIA PLANTARUM, Issue 2 2007Wenlin Yuan Many Frankia strains are pigmented and presumed to produce melanin. However, melanin biosynthesis has yet to be rigorously characterized in Frankia. This study was initiated to determine whether or not Frankia strain CeI5 produced melanin and to identify the biochemical pathway of pigment production. Frankia strain CeI5 first produced a dark pigment in mycelial and other tissue and then in the liquid culture medium when grown in a defined medium containing l -tyrosine. The pigment resisted solvents, lightened when subjected to the action of oxidants, as well as reductants, and produced a flocculent brown precipitate with FeCl3. Spectroscopic characteristics of the extracted pigment were those of melanin. When subjected to gradual dilution, the absorbance decreased unevenly, occurring in the near red range first, then in the visible range, and lastly in the UV range. This observation might resolve the question of why quite different descriptions of melanin UV,visible light absorption spectra exist in the literature. The tyrosinase cofactor copper greatly enhanced melanin biosynthesis at 5.3 × 10,6 M, while 1 × 10,8 M 3,4-dihydroxy- l -phenylalanine hastened pigmentation. The copper-chelating agent KCN and the tyrosinase inhibitor tropolone decreased melanin production at the same concentration of 1 × 10,5 M. This evidence suggests that Frankia strain CeI5 produces melanin via the Raper and Mason pathway. [source] Effects of phenolic compounds isolated from Rabdosia japonica on B16-F10 melanoma cellsPHYTOTHERAPY RESEARCH, Issue 7 2008Teruhiko Nitoda Abstract Pedalitin isolated from the aerial part of Rabdosia japonica (Labiatae), exhibited cytotoxicity against the murine B16-F10 melanoma cell line with an IC50 of 30 µm (9.5 µg/mL). As the cells were cultured with this flavone, melanin production was not suppressed, but rather enhanced. Quercetin isolated from the same source exhibited similar activities, but rutin showed neither activity. Copyright © 2008 John Wiley & Sons, Ltd. [source] Effects of cuminaldehyde on melanoma cellsPHYTOTHERAPY RESEARCH, Issue 6 2008Teruhiko Nitoda Abstract Cuminaldehyde (4-isopropylbenzaldehyde) suppressed melanin formation in cultured murine B16-F10 melanoma cells in a dose-dependent decrease up to 0.25 mm without affecting cell growth. Approximately 30% suppression in melanin production resulted when the cells were cultured with 0.25 mm of cuminaldehyde. This activity was not noticeable with cultured human A375 melanoma cells. Copyright © 2008 John Wiley & Sons, Ltd. [source] Keratinocytes Control the Pheo/Eumelanin Ratio in Cultured Normal Human MelanocytesPIGMENT CELL & MELANOMA RESEARCH, Issue 6 2002Christine Duval The pheo/eumelanin ratio of cultured normal human melanocytes is distinct from the ratio observed for the same cells in vivo where they are in close contact with keratinocytes. To study the possible involvement of keratinocytes in the control of melanogenesis, we compared quantitatively and qualitatively the melanin production in melanocyte mono-cultures, in melanocyte,keratinocyte co-cultures and in pigmented reconstructed epidermis. Pheomelanin and eumelanin contents were assessed by high-performance liquid chromatography with electrochemical and fluorometric detection of their specific degradation products and revealed striking differences in the presence of keratinocytes. In the absence of keratinocytes (melanocyte mono-cultures), we observed a very limited eumelanin production and a very high pheomelanin synthesis. The pheo/eumelanin ratio in mono-cultures could be slightly influenced by changing the composition of the culture medium, however, the very strong imbalance in favor of pheomelanin remained unchanged. An induction of eumelanin synthesis accompanied by an important reduction of pheomelanin formation was only observed in the presence of keratinocytes. The pheo/eumelanin ratio in melanocyte mono-culture dropped from 1043 down to about 25 in the presence of keratinocytes (co-cultures). The same observations were made when the melanocytes were integrated into a reconstructed human epidermis. Interestingly, under co-culture conditions resulting in only a partial contact between melanocytes and keratinocytes, the reduction of the pheo/eumelanin ratio were less pronounced. From these results we conclude that keratinocytes play an important role in the melanin production, affecting the melanogenic pathways. [source] Evaluation of efficacy and safety of rucinol serum in patients with melasma: a randomized controlled trialBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2007A. Khemis Summary Background, Melasma is a hyperpigmentation disorder predominantly affecting sun-exposed areas in women, which is often refractory to treatment. Most commercially available treatments incorporate inhibitors of tyrosinase, a key enzyme in melanin production within the melanocyte. In general, however, the efficacy of these therapies is somewhat limited. Recent studies have identified other enzymes that play an important role in melanogenesis, including tyrosinase-related protein-1 (TRP-1), which catalyses the oxidation of the melanogenetic intermediate 5,6-dihydroxyindole-2-carbolylic acid. Rucinol (4- n -butylresorcinol) has been shown to inhibit the activity of both tyrosinase and TRP-1. Objectives, To assess the efficacy of rucinol serum 0·3% vs. the corresponding vehicle as a treatment for melasma. Secondary objectives were to evaluate local and general tolerability and to assess the skin acceptability of rucinol serum in the target population. Methods, In this prospective, single-centre, double-blind, randomized, vehicle-controlled, bilateral (split-face) comparative trial, 32 women with melasma were provided with two identical tubes containing rucinol serum 0·3% or vehicle. The products were each applied to one-half of the face, according to the randomization scheme, twice daily for 12 weeks (phase 1). A broad-spectrum sunscreen (sun protection factor 60) was also applied daily. Assessments at baseline, 4, 8 and 12 weeks included clinical evaluations by a dermatologist, chromametry, ultraviolet and standard photography, and assessments of skin acceptability and tolerability. After 12 weeks, patients were given the option of an additional 3-month treatment period of open full-face rucinol treatment, with reviews at 16, 20 and 24 weeks (phase 2). Results, Twenty-eight patients completed phase 1 and 26 patients completed phase 2. After 12 weeks, the clinical pigmentation score for rucinol-treated skin was significantly lower than for vehicle-treated skin (P = 0·027). During phase 2, rucinol induced a significant reduction in mean pigmentation score on the half of the face previously treated with vehicle. There was also a further, significant improvement on the rucinol-treated side of the face. Chromametry measurements showed that skin was significantly lighter and less yellow, with a strong trend towards reduced redness, following rucinol therapy compared with vehicle. Rucinol serum showed good tolerability and acceptability and was considered to have good or fair efficacy by 78% of the patient population. Conclusions, Rucinol serum was shown to have significant efficacy compared with vehicle alone in improving melasma after 3 months of treatment, according to clinical and objective assessments of skin colour. [source] Signalling pathways in the pathogenesis of CryptococcusCELLULAR MICROBIOLOGY, Issue 3 2009Lukasz Kozubowski Summary Efficient communication with the environment is critical for all living organisms. Fungi utilize complex signalling systems to sense their environments and control proliferation, development and in some cases virulence. Well-studied signalling pathways include the protein kinase A/cyclic AMP (cAMP), protein kinase C (PKC)/mitogen-activated protein kinase (MAPK), lipid signalling cascades, and the calcium,calcineurin signalling pathway. The human pathogenic basidiomycetous fungus Cryptococcus neoformans deploys sensitive signalling systems to survive in the human host, leading to life-threatening meningoencephalitis. Known virulence traits of this fungus, including the antioxidant melanin production, the antiphagocytic polysaccharide capsule and the ability to grow at 37°C, are orchestrated by complex signalling networks, whose understanding is crucial to better treat, diagnose and prevent cryptococcosis. [source] Cell Shape Normalization, Dendrite Orientation, and Melanin Production of Normal and Genetically Altered (Haploinsufficient NF1)-Melanocytes by Microstructured Substrate InteractionsCHEMPHYSCHEM, Issue 1 2004Simon Jungbauer Abstract Little is known about how functional regulation failure in genetically altered cells is influenced by topographical confinement of cells, a situation often present in tissues in vivo. We used cultured melanocytes derived from human skin samples as a model system for such investigations. Normal melanocytes have a very well defined shape consisting of a cell body and two dendrites arranged 180° relative to each other. In contrast, neurofibromin 1-melanocytes (NF1-melanocytes) have up to a 50,% reduction of neurofibromin 1, which results in an altered morphology that can be easily measured. NF1-melanocytes deviate from the defined structure of normal melanocytes by forming more than two dendrites per cell. We show that morphology consequences of genetically altered melanocytes can be canceled if cells interact with substrates microstructured by stripes that apply mechanophysical signals in the form of physical topography. The strength of the mechanophysical signal was varied systematically by increasing the height of the microstructures. Melanocytes respond to surface topographical features that are larger than 50 nm and have lateral confinements smaller 4 ,m. The response of normal and NF1-melanocytes to different topographies was analyzed quantitatively by determining density distributions for the number of dendrites per cell, the angles between dendrites, and the orientation imprinted in the substrate. The synthesis of melanin, a pigment produced by melanocytes, differs in the case of genetically altered NF1- and normal melanocytes. In both cases, the interaction with microstripes enhanced melanin production significantly. This enhanced melanin production is speculated to be caused by the mechanical stabilization of the dendrites by substrate guidance. [source] | |||||||||||||