Melanogenesis

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Jin-woo Park - One of the best experts on this subject based on the ideXlab platform.

  • Guggulsterone inhibits Melanogenesis in B16 murine melanoma cells by downregulating tyrosinase expression
    International journal of molecular medicine, 2012
    Co-Authors: Jeung-hyun Koo, Byung-hyun Park, Kyoung-suk Rhee, Hyoung-won Koh, Hyun-young Jang, Jin-woo Park
    Abstract:

    In the present study, we investigated the effect of guggulsterone on Melanogenesis in B16 melanoma cells and elucidated its possible mechanism of action. The effects of guggulsterone on Melanogenesis were determined by assaying melanin synthesis and cellular tyrosinase activity in B16/F10 mouse melanoma cells. Guggulsterone dose-dependently inhibited isobutylmethylxanthine (IBMX)-induced Melanogenesis and cellular tyrosinase activity with no cytotoxicity. Decreased melanin biosynthesis was accompanied by the reduced expression of Melanogenesis-related genes, such as tyrosinase, microphthalmia-associated transcription factor, tyrosinase-related protein (TRP)-1 and TRP-2. Guggulsterone also inhibited α-melanocyte stimulating hormone- or forskolin-induced increases in Melanogenesis, suggesting an action on the cAMP-dependent melanogenic pathway. Co-incubation with chenodeoxycholic acid, a well-known farnesoid-X receptor agonist, did not affect IBMX-induced Melanogenesis. These results suggest that guggulsterone exerts a melanogenic inhibitory effect through the downregulation of tyrosinase expression.

  • stimulation of Melanogenesis by scoparone in b16 melanoma cells
    Acta Pharmacologica Sinica, 2006
    Co-Authors: Jeong Yeh Yang, Byung-hyun Park, Jeung-hyun Koo, Kang Beom Kwon, Ju Hyung Lee, Eun Chung Jhee, Younggil Song, Heesook Sohn, Jin-woo Park
    Abstract:

    Aim: The effect of coumarin derivatives on Melanogenesis was investigated in B16 murine melanoma cells. Methods: Melanin content and tyrosinase activity were analyzed spectrophotometrically. The expression of tyrosinase, tyrosinase-related protein-1 (TRP-1) and tyrosinase-related protein-2 (TRP-2) were measured either by reverse transcription-polymerase chain reaction (RT-PCR) or Western blot. Results: Among the coumarin derivatives studied, scoparone (6,7-dimethoxycoumarin) was the most potent; the 6- or 7-methoxy group was found to be essential for the stimulation of Melanogenesis. The melanin content was greatly increased by scoparone in a dose-dependent manner; there was no cytotoxicity at the effective concentrations. Scoparone increased enzyme activity as well as protein and mRNA expression of tyrosinase. In addition, mRNA of TRP-1 and TRP-2 were also increased after treatment with scoparone. H-89, an inhibitor of protein kinase A (PKA), completely inhibited the scoparone-induced increase of Melanogenesis and the tyrosinase protein. Conclusion: These results suggest that scoparone-induced stimulation of Melanogenesis is likely to occur at the transcriptional level of Melanogenesis-related enzymes through PKA signaling.

  • Stimulation of Melanogenesis by glycyrrhizin in B16 melanoma cells.
    Experimental & molecular medicine, 2001
    Co-Authors: Gi-dong Jung, Jeong Yeh Yang, Eun-sup Song, Jin-woo Park
    Abstract:

    Glycyrrhizin (GR), triterpenoid saponin composed of one glycyrrhetinic acid (GA) and two glucuronic acids, is a main constituent of the hydrophilic fraction of licorice (Glycyrrhiza glabra) extracts and is known to have a wide range of pharmacological actions. In this study, we investigated the mechanism of GR effect on Melanogenesis in B16 murine melanoma cells. The cellular levels of tyrosinase mRNA, protein, enzyme activities and melanin contents were increased by GR in a dose dependent manner. Expression of tyrosinase-related protein-2 (TRP-2) mRNA was also increased by GR, however, no significant change was observed on TRP-1. No cytotoxicity was observed at the effective concentration range of GR. GA showed no effect on Melanogenesis at the equivalent nontoxic concentrations, indicating that glycoside structure is important in the stimulatory effect of GR on Melanogenesis. These results indicate that GR-induced stimulation of Melanogenesis is likely to occur through the transcriptional activation.

Byung-tae Choi - One of the best experts on this subject based on the ideXlab platform.

  • Curcumin suppresses α-melanocyte stimulating hormone-stimulated Melanogenesis in B16F10 cells
    International journal of molecular medicine, 2010
    Co-Authors: Jun-hyuk Lee, Ji-yeon Jang, Cheol Park, Byung-woo Kim, Yung Hyun Choi, Byung-tae Choi
    Abstract:

    The present study was designed to assess the potential inhibitory activity of curcumin on the alpha-melanocyte stimulating hormone (alpha-MSH)-stimulated Melanogenesis signal pathway in B16F10 melanoma cells. The molecular mechanism of curcumin-induced inhibitory activity on the alpha-MSH-stimulated Melanogenesis signal pathway, including expression of Melanogenesis-related proteins and activation of Melanogenesis-regulating proteins, was examined in B16F10 cells. Curcumin suppressed the cellular melanin contents and the tyrosinase activity in alpha-MSH-stimulated B16F10 cells. In addition, the expression of Melanogenesis-related proteins such as microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein 1 and 2 was suppressed by curcumin in the alpha-MSH-stimulated B16F10 cells. Notably, a Melanogenesis-regulating signal such as mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) or phosphatidylinositol 3-kinase (PI3K)/Akt was activated by curcumin in the B16F10 cells treated with or without alpha-MSH. The suppressive activity of curcumin on alpha-MSH-induced Melanogenesis was down-regulated by PD98059 and by LY294002. Our results suggest that the suppressive activity of curcumin on alpha-MSH-stimulated Melanogenesis may involve the down-regulation of MITF and its downstream signal pathway through the activation of MEK/ERK or PI3K/Akt.

  • dichloromethane fraction of cimicifuga heracleifolia decreases the level of melanin synthesis by activating the erk or akt signaling pathway in b16f10 cells
    Experimental Dermatology, 2009
    Co-Authors: Ji-yeon Jang, Jun-hyuk Lee, Yung Hyun Choi, Byoung Won Kang, Kyung Tae Chung, Byung-tae Choi
    Abstract:

    Abstract:  Cimicifuga rhizoma has long been used in traditional Korean medicine. In particular, a Cimicifuga heracleifolia extract (CHE) was reported to inhibit the formation of glutamate and the glutamate dehydrogenase activity in cultured rat islet. Glutamate activates Melanogenesis by activating tyrosinase. Accordingly, it was hypothesized that a CHE might inhibit the Melanogenesis-related signal pathways including the inhibition of microphthalmia-associated transcription factor (MITF)-tyrosinase signaling and/or the activation of extracellular signal-regulated kinase (ERK)-Akt signaling. The results showed that CHE inhibits the cellular melanin contents, tyrosinase activity and expression of Melanogenesis-related proteins including MITF, tyrosinase and tyrosinase-related protein (TRP)s in α-melanocyte-stimulating hormone-stimulated B16 cells. Moreover, CHE phosphorylates MEK, ERK1/2 and Akt, which are Melanogenesis inhibitory proteins. The data suggest that CHE inhibits Melanogenesis signaling by both inhibiting the tyrosinase directly and activating the MEK-ERK or Akt signal pathways-mediated suppression of MITF and its downstream signal pathway, including tyrosinase and TRPs. Therefore, C. heracleifolia would be a useful therapeutic agent for treating hyperpigmentation and an effective component in whitening and/or lightening cosmetics.

Jun-hyuk Lee - One of the best experts on this subject based on the ideXlab platform.

  • Curcumin suppresses α-melanocyte stimulating hormone-stimulated Melanogenesis in B16F10 cells
    International journal of molecular medicine, 2010
    Co-Authors: Jun-hyuk Lee, Ji-yeon Jang, Cheol Park, Byung-woo Kim, Yung Hyun Choi, Byung-tae Choi
    Abstract:

    The present study was designed to assess the potential inhibitory activity of curcumin on the alpha-melanocyte stimulating hormone (alpha-MSH)-stimulated Melanogenesis signal pathway in B16F10 melanoma cells. The molecular mechanism of curcumin-induced inhibitory activity on the alpha-MSH-stimulated Melanogenesis signal pathway, including expression of Melanogenesis-related proteins and activation of Melanogenesis-regulating proteins, was examined in B16F10 cells. Curcumin suppressed the cellular melanin contents and the tyrosinase activity in alpha-MSH-stimulated B16F10 cells. In addition, the expression of Melanogenesis-related proteins such as microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein 1 and 2 was suppressed by curcumin in the alpha-MSH-stimulated B16F10 cells. Notably, a Melanogenesis-regulating signal such as mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) or phosphatidylinositol 3-kinase (PI3K)/Akt was activated by curcumin in the B16F10 cells treated with or without alpha-MSH. The suppressive activity of curcumin on alpha-MSH-induced Melanogenesis was down-regulated by PD98059 and by LY294002. Our results suggest that the suppressive activity of curcumin on alpha-MSH-stimulated Melanogenesis may involve the down-regulation of MITF and its downstream signal pathway through the activation of MEK/ERK or PI3K/Akt.

  • dichloromethane fraction of cimicifuga heracleifolia decreases the level of melanin synthesis by activating the erk or akt signaling pathway in b16f10 cells
    Experimental Dermatology, 2009
    Co-Authors: Ji-yeon Jang, Jun-hyuk Lee, Yung Hyun Choi, Byoung Won Kang, Kyung Tae Chung, Byung-tae Choi
    Abstract:

    Abstract:  Cimicifuga rhizoma has long been used in traditional Korean medicine. In particular, a Cimicifuga heracleifolia extract (CHE) was reported to inhibit the formation of glutamate and the glutamate dehydrogenase activity in cultured rat islet. Glutamate activates Melanogenesis by activating tyrosinase. Accordingly, it was hypothesized that a CHE might inhibit the Melanogenesis-related signal pathways including the inhibition of microphthalmia-associated transcription factor (MITF)-tyrosinase signaling and/or the activation of extracellular signal-regulated kinase (ERK)-Akt signaling. The results showed that CHE inhibits the cellular melanin contents, tyrosinase activity and expression of Melanogenesis-related proteins including MITF, tyrosinase and tyrosinase-related protein (TRP)s in α-melanocyte-stimulating hormone-stimulated B16 cells. Moreover, CHE phosphorylates MEK, ERK1/2 and Akt, which are Melanogenesis inhibitory proteins. The data suggest that CHE inhibits Melanogenesis signaling by both inhibiting the tyrosinase directly and activating the MEK-ERK or Akt signal pathways-mediated suppression of MITF and its downstream signal pathway, including tyrosinase and TRPs. Therefore, C. heracleifolia would be a useful therapeutic agent for treating hyperpigmentation and an effective component in whitening and/or lightening cosmetics.

Jeong Yeh Yang - One of the best experts on this subject based on the ideXlab platform.

  • stimulation of Melanogenesis by scoparone in b16 melanoma cells
    Acta Pharmacologica Sinica, 2006
    Co-Authors: Jeong Yeh Yang, Byung-hyun Park, Jeung-hyun Koo, Kang Beom Kwon, Ju Hyung Lee, Eun Chung Jhee, Younggil Song, Heesook Sohn, Jin-woo Park
    Abstract:

    Aim: The effect of coumarin derivatives on Melanogenesis was investigated in B16 murine melanoma cells. Methods: Melanin content and tyrosinase activity were analyzed spectrophotometrically. The expression of tyrosinase, tyrosinase-related protein-1 (TRP-1) and tyrosinase-related protein-2 (TRP-2) were measured either by reverse transcription-polymerase chain reaction (RT-PCR) or Western blot. Results: Among the coumarin derivatives studied, scoparone (6,7-dimethoxycoumarin) was the most potent; the 6- or 7-methoxy group was found to be essential for the stimulation of Melanogenesis. The melanin content was greatly increased by scoparone in a dose-dependent manner; there was no cytotoxicity at the effective concentrations. Scoparone increased enzyme activity as well as protein and mRNA expression of tyrosinase. In addition, mRNA of TRP-1 and TRP-2 were also increased after treatment with scoparone. H-89, an inhibitor of protein kinase A (PKA), completely inhibited the scoparone-induced increase of Melanogenesis and the tyrosinase protein. Conclusion: These results suggest that scoparone-induced stimulation of Melanogenesis is likely to occur at the transcriptional level of Melanogenesis-related enzymes through PKA signaling.

  • Stimulation of Melanogenesis by glycyrrhizin in B16 melanoma cells.
    Experimental & molecular medicine, 2001
    Co-Authors: Gi-dong Jung, Jeong Yeh Yang, Eun-sup Song, Jin-woo Park
    Abstract:

    Glycyrrhizin (GR), triterpenoid saponin composed of one glycyrrhetinic acid (GA) and two glucuronic acids, is a main constituent of the hydrophilic fraction of licorice (Glycyrrhiza glabra) extracts and is known to have a wide range of pharmacological actions. In this study, we investigated the mechanism of GR effect on Melanogenesis in B16 murine melanoma cells. The cellular levels of tyrosinase mRNA, protein, enzyme activities and melanin contents were increased by GR in a dose dependent manner. Expression of tyrosinase-related protein-2 (TRP-2) mRNA was also increased by GR, however, no significant change was observed on TRP-1. No cytotoxicity was observed at the effective concentration range of GR. GA showed no effect on Melanogenesis at the equivalent nontoxic concentrations, indicating that glycoside structure is important in the stimulatory effect of GR on Melanogenesis. These results indicate that GR-induced stimulation of Melanogenesis is likely to occur through the transcriptional activation.

A J Thody - One of the best experts on this subject based on the ideXlab platform.

  • activation of Melanogenesis by vacuolar type h atpase inhibitors in amelanotic tyrosinase positive human and mouse melanoma cells
    FEBS Letters, 2000
    Co-Authors: Janis Ancans, A J Thody
    Abstract:

    In this study, we describe the activation of Melanogenesis by selective vacuolar type H+-ATPase inhibitors (bafilomycin A1 and concanamycin A) in amelanotic human and mouse melanoma cells which express tyrosinase but show no Melanogenesis. Addition of the inhibitors activated tyrosinase within 4 h, and by 24 h the cells contained measurable amounts of melanin. These effects were not inhibited by cycloheximide (2 μg/ml) which is consistent with a post-translational mechanism of activation. Our findings suggest that melanosomal pH could be an important and dynamic factor in the control of Melanogenesis in mammalian cells.

  • Agouti protein can act independently of melanocyte-stimulating hormone to inhibit Melanogenesis.
    Journal of Endocrinology, 1995
    Co-Authors: Gillian Hunt, A J Thody
    Abstract:

    In animals, the coat-darkening effects of alpha-melanocyte stimulating hormone (alpha-MSH) are opposed by agouti protein. Although agouti protein has been shown to be a competitive antagonist of the melanocyte-associated MC-1 melanocortin receptor, the possibility that agouti protein can affect Melanogenesis independently of its ability to antagonise melanocortin activity cannot be excluded. This study demonstrates that murine agouti protein causes both a time- and concentration-dependent suppression of Melanogenesis in B16 F1 murine melanoma cells. In addition, human agouti protein decreases Melanogenesis in cultured human epidermal melanocytes. However, agouti protein has little effect on the ability of alpha-MSH to stimulate Melanogenesis. These observations raise fundamental questions about the mode of action of agouti protein in regulating Melanogenesis.