Norgalanthamine Stimulates Proliferation of Dermal Papilla Cells via Anagen-Activating Signaling Pathways
Autor: | Sang-Pil Yoon, Eun-Sook Yoo, Jung-Il Kang, Sung Min Kim, Hee-Kyoung Kang, Ji-Hoon Kang, Mee Jung Ahn, Young Ho Kim, Ara Ko, Hoon-Seok Yoon, Jin-Won Hyun, Young Sang Koh |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Pharmacology MAPK/ERK pathway integumentary system Chemistry Kinase Pharmaceutical Science General Medicine Cell biology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Hair cycle GSK-3 030220 oncology & carcinogenesis Signal transduction Protein kinase A Protein kinase B PI3K/AKT/mTOR pathway |
Zdroj: | Biological and Pharmaceutical Bulletin. 42:139-143 |
ISSN: | 1347-5215 0918-6158 |
DOI: | 10.1248/bpb.b18-00226 |
Popis: | Norgalanthamine has been shown to possess hair-growth promoting effects, including increase in hair-fiber length in cultured rat vibrissa follicles and increase in dermal papilla cell (DPC) proliferation. However, the intracellular mechanisms that underlie the action of norgalanthamine in DPCs have not been investigated. In this study, we addressed the ability of norgalanthamine to trigger anagen-activating signaling pathways in DPCs. Norgalanthamine significantly increased extracellular signal-regulated kinase (ERK) 1/2 phosphorylation at 0.1 µM, a concentration at which DPC proliferation was also induced. Furthermore, the increases in norgalanthamine-induced ERK 1/2 activation and subsequent DPC proliferation were suppressed by the mitogen-activated protein kinase/ERK kinase (MEK) 1/2 inhibitor, U0126. A 0.1 µM dose of norgalanthamine also increased phosphorylation of AKT, which was followed by an increase in glycogen synthase kinase 3β phosphorylation and nuclear translocation of β-catenin. In addition, LY294002, a phosphatidylinositol 3 kinase (PI3K) inhibitor, blocked the effect of norgalanthamine on DPC proliferation. These results suggest that norgalanthamine can stimulate the anagen phase of the hair cycle in DPCs via activation of the ERK 1/2, PI3K/AKT, and Wnt/β-catenin pathways. |
Databáze: | OpenAIRE |
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