References: Hair growth and hair loss
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.
Carroll JM, McElwee KJ, E King L, Byrne MC, Sundberg JP.
Genetics Institute/Wyeth Research, Cambridge, Massachusetts, USA.
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.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12190862&dopt=Abstract
Exp Dermatol. 2002 Aug;11(4):376-80.
17alpha-estradiol induces aromatase activity in intact human anagen hair follicles ex vivo.
Hoffmann R, Niiyama S, Huth A, Kissling S, Happle R.
Department of Dermatology, Philipp University, Deutschhausstrasse 9, D-35033 Marburg, Germany.
For topical treatment of androgenetic alopecia (AGA) in women, solutions containing either estradiol benzoate, estradiol valerate, 17beta- or 17alpha-estradiol are commercially available in Europe and some studies show an increased anagen and decreased telogen rate after treatment as compared with placebo. At present it is not precisely known how estrogens mediate their beneficial effect on AGA-affected hair follicles. We have shown recently that 17alpha-estradiol is able to diminish the amount of dihydrotestosterone (DHT) formed by human hair follicles after incubation with testosterone, while increasing the concentration of weaker steroids such as estrogens. Because aromatase is involved in the conversion of testosterone to estrogens and because there is some clinical evidence that aromatase activity may be involved in the pathogenesis of AGA, we addressed the question whether aromatase is expressed in human hair follicles and whether 17alpha-estradiol is able to modify the aromatase activity. Herewith we were able to demonstrate that intact, microdissected hair follicles from female donors express considerably more aromatase activity than hair follicles from male donors. Using immunohistochemistry, we detected the aromatase mainly in the epithelial parts of the hair follicle and not in the dermal papilla. Furthermore, we show that in comparison to the controls, we noticed in 17alpha-estradiol-incubated (1 nM) female hair follicles a concentration- and time-dependent increase of aromatase activity (at 24 h: 1 nM = +18%, 100 nM = +25%, 1 micro M = +57%; 24 h: 1 nM = +18%, 48 h: 1 nM = +25%). In conclusion, our ex vivo experiments suggest that under the influence of 17alpha-estradiol an increased conversion of testosterone to 17beta-estradiol and androstendione to estrone takes place, which might explain the beneficial effects of estrogen treatment of AGA.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12190948&dopt=Abstract
Mol Genet Metab. 2002 Aug;76(4):335-9.
The rat shorn mutation (shn) maps between D7Got143 and D7Rat94.
Chrissluis RR, Stoklasek TA, Loman JA, Guariglia A, King TR.
Biological Sciences, Central Connecticut State University, New Britain 06050, USA.
The recessive shorn (shn) mutation in the rat generates an almost complete absence of normal hair. Previous analysis of 85 backcross rats typed for shn-generated hypotrichosis located this marker between the telomere and D7Mgh1 on distal rat Chromosome 7. Here, we present a microsatellite polymorphism analysis of a 184-member backcross panel-including 99 new rats-that places shn within a 2.7cM interval between markers D7Got143 and D7Rat94. In addition, this analysis has allowed meiotic ordering of 18 microsatellite markers-including 10 D7Got markers previously positioned only by radiation reduced hybrid analysis-across the 16.8cM region between D7Mit16 (Cyp2d4) and D7Rat94. Our inability to meiotically separate shn from 8 microsatellite markers (mapped by others over some 2-4cM or more than 40cR of genetic distance) suggests that the shn mutation may result from a chromosomal rearrangement that suppresses recombination throughout this interval.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208139&dopt=Abstract
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