Minoxidil's effect on erk/akt, bcl-2/bax- ratio and DPC

Todd

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(from pubmed: http://www.ncbi.nlm.nih.gov/pubmed/15033191)

Effect of minoxidil on proliferation and apoptosis in dermal papilla cells of human hair follicle.

Han JH, Kwon OS, Chung JH, Cho KH, Eun HC, Kim KH.

Department of Dermatology, Clinical Research Institute, Seoul National University College of Medicine, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, South Korea.
Abstract

BACKGROUND: Minoxidil has been widely used to treat androgenetic alopecia, but little is known about its pharmacological activity or about the identity of its target cells in hair follicles. We hypothesized that minoxidil has direct effects on the proliferation and apoptosis of dermal papilla cells (DPCs) of human hair follicle.

OBJECTIVE: To elucidate the mechanism of topical minoxidil action in terms of stimulating hair growth.

METHODS: We evaluated cell proliferations in cultured DPCs by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and measured the expressions of extracellular signal-regulated kinase (ERK), Akt, Bcl-2, and Bax by Western blot. We also measured elongation of hair follicles in organ culture.

RESULTS: Minoxidil significantly increased the proliferation of DPCs. The levels of ERK phosphorylation and of phosphorylated Akt increased significantly 1 h post-treatment; percentage increase of ERK phosphorylation was 287% at 0.1 microM and 351% at 1.0 microM of minoxidil, and that of Akt phosphorylation was 168% at 0.1 microM and 257% at 1.0 microM of minoxidil. 1.0 microM of minoxidil increased Bcl-2 expression over 150%, while 1.0 microM of minoxidil decreased Bax expression by more than 50%. Moreover, a significant elongation of individual hair follicles in organ culture was observed after adding minoxidil.

CONCLUSION: Minoxidil promotes the survival of human DPCs by activating both ERK and Akt and by preventing cell death by increasing the ratio of Bcl-2/Bax. We suggest that minoxidil stimulates the growth of human hairs by prolonging anagen through these proliferative and anti-apoptotic effects on DPCs.
 

Todd

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This study is interesting for several reasons:
First of all, it sheds some light as to why minoxidil not only grows hair (as has been proven in vitro by VEGF- increase, and K+- channel opening), but also why the anagen phase is prolonged, and why the hair follicle manages to "survive" for so long, even in the presence of DHT.

Secondly; it gives credibility to all of the experimental treatments
that has Bcl-2/bax, dpc proliferation or erk/akt- phosphorylation
(that is green tea, roxitromyicin, tri- peptide copper complex etc) as their mode of action.
Given sufficient absorption into the scalp, these treatments could in theory (I'm not willing to say "would likely") work as well as minoxidil.

The bad news: comparing minoxidil with treatments such as finasteride and dutasteride, it's clear that despite keeping those cells alive, and keeping the anagen phase going for as long as possible; preventing (or even simply lowering) androgen stimulation (DHT) has a much greater effect on both hair survival and hair growth than directly stimulating DPC's. (NB: minoxidil GROWS more hair than finasteride per square inch, but doesn't manage to maintain as much, resulting in a netto lower hair count over time)
However, minoxidil's effect is still not to be ignored, it does indeed stimulate growth and apparently does so in a much more sophisticated way than the researchers first thought.
 
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