Study: Minoxidil helps inhibit apoptosis (programmed cell death) in hair follicles,
"Minoxidil helps inhibit apoptosis (programmed cell death) in hair follicles, according to this new study below. Hair follicles undergo massive apoptosis when switching from anagen to catagen.
One of the hallmarks of MPB is a decrease in the length of anagen. So, it would seem that minoxidil is capable of countering this specific aspect of pattern baldness (i.e., short anagen phases). The study below also notes that minoxidil increases the proliferation rate of dermal papilla cells (this also likely contributes to lengthening of anagen)." from Almighty in HairSite's Men's Forum.
J Dermatol Sci. 2004 Apr;34(2) 1-8.
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.
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 0.1microM and 351% at 1.0microM of minoxidil, and that of Akt phosphorylation was 168% at 0.1microM and 257% at 1.0microM of minoxidil. 1.0microM of minoxidil increased Bcl-2 expression over 150%, while 1.0microM 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.
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