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We investigated the characteristics of F-doped SnO 2 (FTO)/Ag/FTO films prepared using thermal evaporation at room temperature for the application of the as-formed films in transparent thin film heaters (TFHs) of automobiles. To optimize the electrical and optical properties of the FTO/Ag/FTO multi-layer, the figure of merit (FoM) values of the FTO/Ag/FTO multi-layers were compared as a function of the thickness of the Ag and FTO layers. The sheet resistance and optical transmittance of the FTO/Ag/FTO multi-layer were primarily affected by the Ag inter-layer and bottom/top FTO thicknesses, respectively. At optimized Ag (10 nm) and FTO (40 nm) thicknesses, we fabricated a FTO/Ag/FTO electrode with a sheet resistance of 8.00 Ohm/square, an optical transmittance of 83.04 % at a visible wavelength (400–800 nm) and a FoM value of 19.49 Ohm-1. The TFHs comprising the optimal FTO/Ag/FTO electrode exhibited a saturated temperature of 117 °C at a low operating direct current of 6 V, owing to the low sheet resistance. In addition, the FTO/Ag/FTO-based TFHs exhibited thermally stable performances owing to the stability of the bottom and top FTO electrodes. The performance of the FTO/Ag/FTO-based TFHs demonstrated that the thermally evaporated FTO/Ag/FTO multi-layer is a promising, stable, and transparent electrode material for application in the front window TFHs used in automobiles. [ABSTRACT FROM AUTHOR]

We developed a one-step simple wet etching process for flexible Ga, Ti co-doped In 2 O 3 (IGTO)/AgPdCu (APC)/IGTO multi-layer electrodes deposited on colorless polyimide (CPI) substrates for flexible bottom emission organic light-emitting diodes (OLEDs). To fabricate OLEDs, the transparent and flexible IGTO/APC/IGTO multilayer electrode with a low sheet resistance of 8.35 Ohm/square and high average transmittance of 82.65 % was directly patterned using a mixed etchant of oxalic acid and nitric acid. For direct patterning of the IGTO/APC/IGTO electrode, wet etching condition was optimized as a function of etch rate, mixture solution ratio, and process temperature. At optimal wet etching condition with oxalic acid of 1 M and nitric acid of 0.79 M at 30 ℃, we successfully patterned the IGTO/APC/IGTO multi-layer without residue by one-step wet etching process. To demonstrate the feasibility of one-step patterned IGTO/APC/IGTO bottom electrode, we fabricated typical bottom emission (OLEDs) on the patterned IGTO/APC/IGTO electrodes. The performance of the flexible OLEDs with the patterned IGTO/APC/IGTO multi-layer electrodes was similar to that of rigid OLEDs with reference ITO electrodes, demonstrating the effectiveness of one-step wet etching as an effective patterning process for flexible IGTO/APC/IGTO multi-layer electrodes. [Display omitted] • Transparent and flexible InGaTiO/AgPdCu/InGaTiO multilayer electrodes. • One-step wet etching of InGaTiO/AgPdCu/InGaTiO multilayer for direct patterning • Outstanding mechanical flexibility of InGaTiO/AgPdCu/InGaTiO multilayer electrodes. • Transparent InGaTiO/AgPdCu/InGaTiO anode for flexible organic light emitting diodes [ABSTRACT FROM AUTHOR]

Objectives Previously, we reported that sphingosine-1-phosphate (S1P) reduced melanin synthesis. In this study we have investigated S1P receptor-mediated extracellular signal-regulated protein kinase (ERK) activation and microphthalmia-associated transcription factor (MITF) phosphorylation. Methods To examine S1P-induced signalling pathways, electron and confocal microscopic studies, reverse transcription-polymerase chain reaction and Western blot analysis were performed. Key findings S1P phosphorylated MITF at Ser73, which may have resulted in a MITF mobility shift. Furthermore, 90 kDa ribosomal S6 kinase-1 (RSK-1) phosphorylation was observed after S1P treatment. In addition, PD98059 abrogated the S1P-induced MITF mobility shift and RSK-1 activation. In experiments with MITF mutants, it was shown that dual phosphorylation at Ser73 and Ser409 was indispensable for MITF degradation. We investigated further the actions of S1P on its specific receptors. The results showed that pertussis toxin completely abolished the hypopigmentary effects and ERK pathway activation by S1P, suggesting that S1P regulated melanogenesis via its receptor. The use of specific receptor antagonists indicated that the S1P3 receptor was dominantly involved in S1P-induced ERK activation and hypopigmentation. Conclusions The results suggested that S1P reduced melanin synthesis via S1P3 receptor-mediated ERK and RSK-1 activation, and subsequent MITF dual phosphorylation and degradation. [ABSTRACT FROM AUTHOR]

Objectives Sphingolipids act as structural components in cell membranes, and form lipid intermediates that have functional roles as signalling molecules in various cellular processes. Our previous findings have suggested that sphingolipid metabolites are deeply involved in the regulation of melanogenic processes. In this study we aimed to examine sphingosylphosphorylcholine-mediated signalling pathways related to melanogenesis. Methods We determined the hypopigmenting effects and the related signalling pathways of sphingosylphosphorylcholine in Mel-Ab cells. In particular, we analysed the involvement of the G-protein-coupled receptor in sphingosylphosphorylcholine-induced MITF degradation. Key findings Western blotting revealed that sphingosylphosphorylcholine induced the activation of extracellular signal-regulated kinase (ERK), as well as Akt. Moreover, the specific Akt pathway inhibitor LY294002 blocked the hypopigmenting effect of sphingosylphosphorylcholine and abrogated the sphingosylphosphorylcholine-mediated down-regulation of microphthalmia-associated transcription factor (MITF), showing that the Akt pathway is involved in sphingosylphosphorylcholine-mediated melanin inhibition. Treatment with the proteasome inhibitor MG132 blocked the decrease in MITF by sphingosylphosphorylcholine, but sphingosylphosphorylcholine did not decrease the level of MITF mRNA, indicating that the reduction in the level of MITF results from MITF degradation. Furthermore, pre-incubation of Mel-Ab cells with pertussis toxin completely abolished the hypopigmenting effects and the activation of ERK and Akt by sphingosylphosphorylcholine, suggesting that the effects of sphingosylphosphorylcholine are mainly dependent on the G-protein-coupled receptor). Conclusions Together, these results suggest that sphingosylphosphorylcholine reduces melanin synthesis via pertussis toxin-sensitive ERK and Akt activation, and subsequent MITF degradation. [ABSTRACT FROM AUTHOR]

Abstract: In the present study, we investigated the effects of heat treatment on melanogenesis in a mouse melanocyte cell line (Mel-Ab). It has been reported that activated extracellular signal-regulated kinase (ERK) is responsible for microphthalmia-associated transcription factor (MITF) degradation, which leads to a reduction in tyrosinase protein production and melanin synthesis. Here we demonstrate that heat treatment induces sustained ERK activation, which may inhibit melanogenesis. However, the specific ERK pathway inhibitors, PD98059 or U0126 did not restore heat-induced hypopigmentation. Furthermore, PD98059 or U0126 hardly blocked the heat-induced activation of ERK. These results suggest that heat treatment may inactivate protein phosphatase, and thus ERK activation is maintained. To support this hypothesis, we examined the effects of heat treatment on protein phosphatase 2A (PP2A) activity. The results obtained show that heat treatment inactivates PP2A, which may subsequently cause ERK activation and that heat treatment inhibits MITF promoter activity. Overall, our results demonstrate that heat treatment reduces melanin production in a temperature-dependent manner. [Copyright &y& Elsevier]

Transforming growth factor-β1 (TGF-β1) plays a pivotal role in cell proliferation, differentiation, and apoptosis. In this study, we investigated the effects of TGF-β1 on melanogenesis using a spontaneously immortalized mouse melanocyte cell line, Mel-Ab. Our results show that TGF-β1 significantly inhibits melanin synthesis in a concentration-dependent manner and that it reduces the activity of tyrosinase, the rate-limiting melanogenic enzyme. We also found that TGF-β1 reduces microphthalmia-associated transcription factor (MITF) promoter activity and decreased MITF, tyrosinase, tyrosinase-related protein-1 (TRP-1), and TRP-2 protein production. In addition, TGF-β1 was found to induce a delay in the activation of extracellular signal-regulated kinase (ERK) at 6 h, whereas many growth factors activate ERK transiently in minutes. Moreover, the specific ERK pathway inhibitor, PD98059 blocked the hypopigmenting effects induced by TGF-β1. PD98059 was also found to abrogate the TGF-β1-mediated down-regulation of MITF, tyrosinase, TRP-1, and TRP-2 production. These results suggest that the ERK pathway may be involved in the melanogenic signaling cascade, and that delayed ERK activation by TGF-β1 contributes to reduced melanin synthesis via MITF down-regulation. [Copyright &y& Elsevier]

In this study, we investigated the effects of lysophosphatidic acid (LPA) on melanogenesis in Mel-Ab cells. We found that LPA significantly attenuates melanin synthesis, and reduces the activity of tyrosinase, the rate-limiting melanogenic enzyme. Interestingly, LPA was also found to induce the activation of a 90 kDa ribosomal S6 kinase (RSK-1), which is known to phosphorylate microphthalmia-associated transcription factor (MITF) at serine 409. Though it has been previously reported that the phosphorylation of MITF is followed by the degradation of MITF, we found that LPA significantly inhibited MITF promoter activity, and that this reduced MITF and tyrosinase protein production. Our results indicate that LPA contributes to reduced melanin synthesis via the down-regulation of MITF. [Copyright &y& Elsevier]

We investigated the effect of hydrogen doping on characteristics of InGaTiO (IGTO) electrode with high conductivity and transmittance during sputtering process. After hydrogen doping, the 300 nm-thick IGTO:H electrode showed lower sheet resistance of 13.79 Ω/square compared to sheet resistance (69.2 Ω/square) of pure IGTO electrode without change of optical transmittance. In addition, wet etching reaction rate of IGTO:H electrode for patterning process was significantly accelerated after hydrogen doping. Possible explanation for hydrogen doping effect on electrical properties and wet etching process of the IGTO:H electrode was suggested. The doped hydrogen influenced the electrical characteristics through the passivation of dangling bonds and oxygen vacancies. Moreover, it significantly impacts crystalline structure, consequently altering the etching rate. Using patterned IGTO:H electrodes, we fabricated red organic light emitting diodes (OLEDs) to show feasibility of the IGTO:H electrodes. External quantum efficiency and current efficiency of the red OLED with IGTO:H (10%) were higher than IGTO electrode without hydrogen doping, indicating that hydrogen doping is an effective method to improve the film properties and IGTO:H electrode can serve as a prospective transparent anode for both flexible and rigid OLEDs. [Display omitted] • Highly conductive and transparent hydrogen-doped InGaTiO electrodes (IGTO:H). • Possible mechanism of the effect of hydrogen doping on the electrical properties and wet-etching rate of IGTO:H electrode. • IGTO:H electrodes exhibit enhanced electrical and mechanical properties after hydrogen doping. • Transparent IGTO:H electrodes for red organic light emitting diodes. [ABSTRACT FROM AUTHOR]

Cyclooxygenase-2 (COX-2) appears to play an important role in inflammation and carcinogenesis, and 2,2′-azobis (2-amidinopropane) dihydrochloride (AAPH) is a hydrophilic azo compound known to generate free radicals. Because reactive oxygen species (ROS) are known to elevate COX-2 expression, we evaluated the effect of AAPH on the expression of COX-2 in a human keratinocyte cell line, HaCaT. When cells were exposed to AAPH, marked COX-2 induction was observed. To clarify the signaling mechanism involved, we next investigated the effects of AAPH upon three major subfamilies of the mitogen-activated protein kinases (MAPKs). AAPH caused an increase in the phosphorylation of extracellular signal-regulated kinase (ERK), p38 and c-Jun NH2-terminal kinase (JNK). Furthermore, we found that PD98059, an ERK pathway inhibitor, and SB203580, a p38 MAPK inhibitor, diminished AAPH-induced COX-2 expression and PGE2 production, whereas JNK inhibitor did not suppress COX-2 expression or PGE2 production by AAPH. These findings suggest that the ERK and p38 MAPK pathways, but not the JNK pathway, are involved in AAPH-induced inflammatory progression. In addition, we found that both the water-soluble Vitamin E derivative, Trolox, and the green tea constituent, (−)-epigallocatechin gallate (EGCG), diminished AAPH-induced COX-2 expression and p38 activation. [Copyright &y& Elsevier]

Summary: Background: Melanogenesis is regulated by a series of enzymes under the control of microphthalmia-associated transcription factor (MITF). Objective: The aim of this study was to examine melanosome-associated protein levels in Mel-Ab cells after hinokitiol treatment. Methods: We measured melanin contents and analyzed melanosome-associated protein levels using Western blot and RT-PCR analysis. Results: Hinokitiol markedly inhibited melanin synthesis and also reduced the protein levels of tyrosinase (TYR), tyrosinase-related protein 1 (TYRP-1), tyrosinase-related protein 2 (TYRP-2) and MITF in Mel-Ab cells. In addition, hinokitiol significantly increased the phosphorylations of extracellular signal-regulated kinases 1 and 2 (ERK1/2). Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that TYR and MITF mRNA levels were significantly decreased but that levels of TYRP-1 and TYRP-2 mRNA were unaffected by hinokitiol treatment. These results suggest that hinokitiol-induced ERK phosphorylation reduces MITF and TYR transcription, and mediates the action of hinokitiol on melanogenesis. Interestingly, the mRNAs of TYRP-1 and TYRP-2 were unaffected, although the protein levels of TYRP-1 and TYRP-2 were down-regulated. Thus, the effects of hinokitiol on the transcription of TYR may differ from its effects on TYRP-1 and TYRP-2. Conclusion: Therefore, we suggest that TYRP-1 and TYRP-2 may be regulated by post-translational degradation after hinokitiol treatment. [Copyright &y& Elsevier]