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Curr Biol 2003 Feb 18;13(4):333-8
Notch/RBP-J Signaling Regulates Epidermis/Hair Fate Determination of Hair Follicular Stem Cells.
Notch signaling is involved in the cell fate determination of various cell lineages. Notch interaction with its ligand induces the cleavage of its intracellular domain (IC), and the Notch IC translocates to the nucleus and binds to RBP-J to transactivate transcription of target genes. All four Notches in mammals bind to RBP-J to exert their transactivation activities. Notch is expressed in developing or differentiating epidermis and hairs, inhibits the terminal differentiation of the epidermis, and regulates hair differentiation. The common stem cells that reside in the upper portion of hair follicles (the bulge) contribute to epidermal and hair cell formation. However, it is unknown what determines whether hair follicular stem cells will become hairs or epidermis. Here we report that conditionally disrupting the mouse RBP-J gene in a mosaic pattern to avoid embryonic lethality of RBP-J-deficiency caused hair loss, epidermal hyperkeratinization, and epidermal cyst formation. Cyst formation is probably due to a combination of the aberrant fate determination of RBP-J-deficient stem cells to epidermal progenitors and their accelerated differentiation into epidermis. These results suggest that Notch/RBP-J signaling regulates the cell fate determination of hair follicular stem cells at the bulge region.
Mol Cell Endocrinol 2002 Dec 30;198(1-2):89-95
Androgens and alopecia.
Androgens have profound effects on scalp and body hair in humans. Scalp hair grows constitutively in the absence of androgens, while body hair growth is dependent on the action of androgens. Androgenetic alopecia, referred to as male pattern hair loss (MPHL) in men and female pattern hair loss (FPHL) in women, is due to the progressive miniaturization of scalp hair. Observations in both eunuchs, who have low levels of testicular androgens, and males with genetic 5alpha-reductase (5alphaR) deficiency, who have low levels of dihydrotestosterone (DHT), implicate DHT as a key androgen in the pathogenesis of MPHL in men. The development of finasteride, a type 2-selective 5alphaR inhibitor, further advanced our understanding of the role of DHT in the pathophysiology of scalp alopecia. Controlled clinical trials with finasteride demonstrated improvements in scalp hair growth in treated men associated with reductions in scalp DHT content, and a trend towards reversal of scalp hair miniaturization was evident by histopathologic evaluation of scalp biopsies. In contrast to its beneficial effects in men, finasteride did not improve hair growth in postmenopausal women with FPHL. Histopathological evaluation of scalp biopsies confirmed that finasteride treatment produced no benefit on scalp hair in these women. These findings suggest that MPHL and FPHL are distinct clinical entities, with disparate pathophysiologies. Studies that elucidate the molecular mechanisms by which androgens regulate hair growth would provide greater understanding of these differences.
Clin Exp Dermatol 2002 Jul;27(5):410-7
Alopecia areata - animal models.
Several rodent models with spontaneous and induced alopecia areata (AA), a nonscarring inflammatory hair loss disease with suspected autoimmune elements, have been identified. Of these, the C3H/HeJ mouse and DEBR rat have been most extensively used in examining AA development. Flow cytometry and micro array characterization, manipulation of inflammatory cells by in vivo cell depletion or cell receptor blockade, lymph node cell transfer between affected and unaffected rodents, and the recent use of transgenic knockout mice have given important insights into the development of AA. From our current understanding of rodent models, the development of AA relies upon a general genetic susceptibility where major susceptibility genes may be supplemented by minor disease severity modifying genes. However, the actual onset of AA, its duration, extent, and persistence in individual rodents may be modified by epigenetic factors. Rodent AA seems to be fundamentally, but not exclusively, Th1 cell mediated. Onset of disease may be dependent on several factors including the break down of the putative anagen stage hair follicle immune privilege, appropriate antigen presentation with costimulation of lymphocytes, presence of autoreactive lymphocytes, and a deficiency of functional immune system regulatory cells. Rodents have already been used in examining a variety of current AA treatments and developing new therapies with some success. With a greater understanding of AA disease mechanisms through rodent model research, improved and more specific treatment interventions may be defined.
Clin Exp Dermatol 2002 Jul;27(5):405-9
Epidemiology and genetics of alopecia areata.
The frequency of alopecia areata and observed patterns of heritability are in keeping with a polygenic inheritance model but the genetics of alopecia areata is still poorly understood. The role of environmental factors in triggering disease initiation or exacerbation remains almost entirely speculative. Using the candidate gene approach, three susceptibility/severity factors have been identified. HLA alleles were the first to show a strong association with alopecia areata and some DQB and DR alleles have been demonstrated to confer a high risk for disease by both case-control and family-based studies. Interleukin (IL)-1 cluster genes, mainly the IL-1 receptor antagonist, show a strong association with disease severity in alopecia areata and a number of other autoimmune and inflammatory diseases. Finally, the association of alopecia areata with Down's syndrome, the high frequency of alopecia areata in autoimmune polyglandular syndrome type I due to mutations of the autoimmune regulator (AIRE) gene on chromosome 21q22.3 and the finding of association with MX1, another gene in the Down's syndrome region of chromosome 21 indicate this area of the genome as a promising target for future-family based investigations. The role of individual genes of the MHC, IL-1 cluster or chromosome 21q22.3 is difficult to establish and further genetic and functional investigations are needed to confirm their involvement in the pathogenesis of alopecia areata.
Hair growth is a sophisticated biological process, which is still not thoroughly understood.
A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the diversity of the problems underlying hair loss, there is no single solution for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.
Hair Million is an alternative solution to hair loss problems. Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss for a fraction of people who take it. We do not know the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth.
We only know by anecdotal observations. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth.
For the clinically tested, FDA approved prescription medication, check Propecia.
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