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Scopoletin Stimulates Melanogenesis via cAMP/PKA Pathway and Partially p38 Activation

Scopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse rel... Full description

Journal Title: Biological and Pharmaceutical Bulletin 2017, Vol.40(12), pp.2068-2074
Main Author: Dae-Sung Kim(A
Other Authors: Su-Bin Cha(A , Min-Cheol Park(B , Seol-A Park(C , Hye-Soo Kim(D , Won-Hong Woo(E , Yeun-Ja Mun(A
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0918-6158
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recordid: meteomoecs7biolo/2017/004012/008/2068-2074
title: Scopoletin Stimulates Melanogenesis via cAMP/PKA Pathway and Partially p38 Activation
format: Article
creator:
  • Dae-Sung Kim(A
  • Su-Bin Cha(A
  • Min-Cheol Park(B
  • Seol-A Park(C
  • Hye-Soo Kim(D
  • Won-Hong Woo(E
  • Yeun-Ja Mun(A
subjects:
  • scopoletin
  • tyrosinase
  • microphthalmia-associated transcription factor
  • cAMP
  • p38 mitogen-activated protein kinase
  • small interfering RNA
  • Scopoletin
  • Tyrosinase
  • Microphthalmia-Associated Transcription Factor
  • Camp
  • P38 Mitogen-Activated Protein Kinase
  • Small Interfering Rna
ispartof: Biological and Pharmaceutical Bulletin, 2017, Vol.40(12), pp.2068-2074
description: Scopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by protein kinase A (PKA) inhibitors (H-89 and KT5720), while a protein kinase C (PKC) inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by small interfering RNA (siRNA) decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.
language: eng
source:
identifier: ISSN: 0918-6158
fulltext: fulltext
issn:
  • 09186158
  • 0918-6158
url: Link


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titleScopoletin Stimulates Melanogenesis via cAMP/PKA Pathway and Partially p38 Activation
creatorDae-Sung Kim(A ; Su-Bin Cha(A ; Min-Cheol Park(B ; Seol-A Park(C ; Hye-Soo Kim(D ; Won-Hong Woo(E ; Yeun-Ja Mun(A
ispartofBiological and Pharmaceutical Bulletin, 2017, Vol.40(12), pp.2068-2074
identifierISSN: 0918-6158
descriptionScopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by protein kinase A (PKA) inhibitors (H-89 and KT5720), while a protein kinase C (PKC) inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by small interfering RNA (siRNA) decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.
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subjectscopoletin ; tyrosinase ; microphthalmia-associated transcription factor ; cAMP ; p38 mitogen-activated protein kinase ; small interfering RNA ; Scopoletin ; Tyrosinase ; Microphthalmia-Associated Transcription Factor ; Camp ; P38 Mitogen-Activated Protein Kinase ; Small Interfering Rna;
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titleScopoletin Stimulates Melanogenesis via cAMP/PKA Pathway and Partially p38 Activation
descriptionScopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by protein kinase A (PKA) inhibitors (H-89 and KT5720), while a protein kinase C (PKC) inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by small interfering RNA (siRNA) decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.
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abstractScopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by protein kinase A (PKA) inhibitors (H-89 and KT5720), while a protein kinase C (PKC) inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by small interfering RNA (siRNA) decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.
pubPharmaceutical Society of Japan
urlhttp://mol.medicalonline.jp/en/journal/download?GoodsID=cs7biolo/2017/004012/008&name=2068-2074e
doi10.1248/bpb.b16-00690
eissn13475215