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Dermatology 2003;206(2):85-95
Steroidogenic isoenzymes in human hair and their potential role in androgenetic alopecia.
Androgenetic alopecia (AGA) is the most common type of hair loss. The relatively strong concordance of the degree of baldness in fathers and sons is not consistent with a simple Mendelian trait, and a polygenic basis is considered to be most likely. So far, the predisposing genes for AGA are unknown and we do not understand the molecular steps involved in androgen-dependent beard growth versus androgen-dependent hair loss, but AGA can be defined as a dihydrotestosterone (DHT)-dependent process with continuous miniaturization of sensitive hair follicles. The type 2 5alpha-reductase plays a central role by the intrafollicular conversion of testosterone to DHT. However, due to the increasing knowledge in this field, we now know that there are many more steroidogenic enzymes involved in the onset and development of AGA, and this article shall provide a critical overview of recent discoveries.
Ann Dermatol Venereol 2002 May;129(5 Pt 2):787-92
Hormonal interaction and hair growth
Androgenetic alopecia (AGA) is the most common form of hair loss in men and women. This continuous process results in a form of alopecia that follows a definite pattern in those individuals who are genetically predisposed. Although clinically different, the pathogenetic pathways leading to this type of hair loss are thought to be similar in both sexes. A genetic predisposition is a feature of AGA, but the predisposing genes are still unknown. Our understanding, however, of the hormonal effects on hair growth is far more advanced. AGA can be defined as a dihydrotestosterone (DHT)-dependent process with continuous miniaturization of sensitive hair follicles. So far, we do not understand the molecular steps involved in androgen-dependent beard growth versus androgen-dependent hair loss. However, the local androgen metabolism plays a central role in the intrafollicular conversion of weak androgens, such as DHEAS, to more potent androgens such as T or DHT within the hair follicle. The dermal papilla plays a central role by exhibiting an array of important steroidogenic isoenzymes. Provided that the dermal papilla (DP) cell triggers and regulates the growth of hair follicles, this physiological role may be reflected by metabolic differences, which could account for differences in androgen sensitivity as observed in hair follicles from different body sites, and in conditions such as male pattern baldness. The observation of STS, 17beta-HSD, 3beta-HSD, 3alpha-HSD and type 2 5alpha-R-activity within the DP could be a clue to understanding the regulation of androgen action in the human hair follicle by local androgen modification on target cell level. Hence, some of the intrafollicular steroidogenic enzymes would be potential pharmaceutical targets for the treatment of AGA or hirsutism.
J Invest Dermatol 2002 Aug;119(2):392-402
Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.
Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6, and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42 known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast, 114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies. In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.
Dermatol Clin 2001 Oct;19(4):711-26, ix
Hair and systemic disease.
Hair loss (alopecia) occurs as a manifestation of numerous systemic diseases, but usually can be categorized into one of five general groups: telogen effluvium, anagen arrest, follicular destruction, hair miniaturization, and hair shaft defects. An excess of hair also can be evidence of internal disease, and there are two general categories of increased hair density: hypertrichosis and hirsutism. The basic categories of hair disease and the systemic conditions associated with them are discussed. The history, physical examination, and histopathologic data usually are sufficient to categorize the form of hair disorder and may provide a clue to the nature of the underlying systemic disease.
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