Keratinocyte growth inhibition through the modification of W


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Evening all.
Been a while since I dropped by. This study is quite interesting. Seems to affirm the role of wnt signalling in male pattern baldness and for the first time hints that the DHT/androgen receptorcomplex is actually binding to beta-catenin and altering/lowering beta-catenin levels as i understand from this abstract.

J Clin Endocrinol Metab. 2009 Jan 13. [Epub ahead of print] Links
Keratinocyte growth inhibition through the modification of Wnt signaling by androgen in balding dermal papilla cells.

Kitagawa T, Matsuda KI, Inui S, Takenaka H, Katoh N, Itami S, Kishimoto S, Kawata M.
Department of Dermatology Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; Department of Anatomy and Neurobiology Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan; Department of Regenerative Dermatology, Graduate School of Medicine Osaka University, Osaka, Japan.
Context/Objective: Androgen induces androgenetic alopecia (Androgenetic Alopecia) which has a regressive effect on hair growth from the frontal region of the scalp. Conversely, Wnt proteins are known to positively affect mammalian hair growth. We hypothesized that androgen reduces hair growth via an interaction with the Wnt signaling system. The objective of this study was to investigate the effect of androgen on Wnt signaling in dermal papilla (DP) cells. Design: The effect of androgen and Wnt3a on keratinocyte (KC) proliferation was measured by use of a co-culture system consisting of DP cells and KCs. The molecular mechanisms of androgen and Wnt pathway interactions in DP cells were examined by analyzing the expression, intracellular localization and activity of the androgen receptor (AR) and also down-stream Wnt signaling molecules. Results: Wnt3a-dependent keratinocyte growth was suppressed by the addition of dihydrotestosterone (DHT) in coculture with DP cells that were derived from Androgenetic Alopecia patients, but growth was not suppressed in coculture with DP cells from non-Androgenetic Alopecia males. While DP cells from both scalp regions expressed AR protein, the expression levels of AR and co-translocation with beta-catenin, a down stream Wnt signaling molecule, were higher in DP cells of Androgenetic Alopecia patients than in DP cells from non-Androgenetic Alopecia males. In addition, significant suppression of Wnt signal-mediated transcription in response to DHT treatment was observed only in DP cells from Androgenetic Alopecia patients. Conclusion: These results suggest that Wnt signaling in DP cells is regulated by androgen and this regulation plays a pivotal role in androgen's action on hair growth.


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Wow...very interesting research and it definitely backs up Elaine Fuchs & Dr. Cotsarelis' research as well. So what does this mean in terms of a cure? Is Wnt just suppressed due to the continuing action of DHT or is it permantently turned off/down? If it was the former then DHT inhibition should regrow our hair back, so it's probably the later.

Harold (or anyone else), do you have any knowledge about Wnt signaling. I was just mentioning this on another forum that I'm certain Wnt is the critical component we really need to look at, instead of EGFR inhibitors. I doubt the current DIY method of mixing lithium oratate/chloride in DMSO has any effect on Wnt signaling. We really need a mechanism that ensures upregulation of Wnt in the scalp/follicles, does anyone know anything about that?