Copiaincollato da Regrowth visto che lo studio originale non lo trovo...[
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Interaction of Androgen Receptor With Wnt Signaling Axis in Dermal Papilla Cells Kitagawa, Tomoko;1 Matsuda, Ken-ichi;2 Inui, Shigeki;3 Takenaka, Hideya;1 Katoh, Norito;1 Itami, Satoshi;3 Kawata, Mitsuhiro;2 Kishimoto, Saburo;
1. Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; 2. Department of Anatomy and Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; 3. Department of Regenerative Dermatology, Osaka University of Medicine, Suita, Japan
Objective: Wnt and androgen are known to positively and negatively affect mammalian hair growth. We hypothesized that androgen reduces hair growth through the interaction with Wnt signaling system. The purpose of this study is to investigate the effect of androgen on Wnt signaling in dermal papilla cells (DPCs).
Approach: The effect of androgen and Wnt3a on keratinocytes (KCs) proliferation was measured using coculture system of DPCs and KCs. Molecular mechanism of interaction of androgen and Wnt signals in DPCs was examined by analyzing the expression, intracellular localization and activities of androgen receptor (AR) and down-stream molecules of Wnt signaling. We also studied the expression level of TGF-beta in DPCs by real-time PCR analysis.
Results: Wnt3a stimulated the growth of KCs when cocultured with DPCs. Wnt3a-dependent growth of KCs was suppressed by androgen in male-derived DPCs (MDPCs) co-culture, but not in female derived DPCs co-culture. Androgen treatment suppressed Wnt-mediated transcription and promoted the expression of TGF-beta in MDPCs. While both of male- and female-derived DPCs expressed AR, the expression level and the degree of nuclear translocation of AR were higher in MDPCs.
Conclusion: These results strongly suggest that the inhibitory action of androgen on KC proliferation in the co-culture is mediated through the suppression of Wnt signaling as well as TGF-beta production by AR in in MDPCs.
Ciao
MA - r l i n
]Interaction of Androgen Receptor With Wnt Signaling Axis in Dermal Papilla Cells Kitagawa, Tomoko;1 Matsuda, Ken-ichi;2 Inui, Shigeki;3 Takenaka, Hideya;1 Katoh, Norito;1 Itami, Satoshi;3 Kawata, Mitsuhiro;2 Kishimoto, Saburo;
1. Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; 2. Department of Anatomy and Neurobiology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; 3. Department of Regenerative Dermatology, Osaka University of Medicine, Suita, Japan
Objective: Wnt and androgen are known to positively and negatively affect mammalian hair growth. We hypothesized that androgen reduces hair growth through the interaction with Wnt signaling system. The purpose of this study is to investigate the effect of androgen on Wnt signaling in dermal papilla cells (DPCs).
Approach: The effect of androgen and Wnt3a on keratinocytes (KCs) proliferation was measured using coculture system of DPCs and KCs. Molecular mechanism of interaction of androgen and Wnt signals in DPCs was examined by analyzing the expression, intracellular localization and activities of androgen receptor (AR) and down-stream molecules of Wnt signaling. We also studied the expression level of TGF-beta in DPCs by real-time PCR analysis.
Results: Wnt3a stimulated the growth of KCs when cocultured with DPCs. Wnt3a-dependent growth of KCs was suppressed by androgen in male-derived DPCs (MDPCs) co-culture, but not in female derived DPCs co-culture. Androgen treatment suppressed Wnt-mediated transcription and promoted the expression of TGF-beta in MDPCs. While both of male- and female-derived DPCs expressed AR, the expression level and the degree of nuclear translocation of AR were higher in MDPCs.
Conclusion: These results strongly suggest that the inhibitory action of androgen on KC proliferation in the co-culture is mediated through the suppression of Wnt signaling as well as TGF-beta production by AR in in MDPCs.
Ciao
MA - r l i n