References: Hair growth and hair loss
Am J Dermatopathol. 1997 Jun;19(3):254-7.
bcl-2 expression in pilomatricoma.
Farrier S, Morgan M.
Department of Pathology, University of South Florida College of Medicine, Tampa, USA.
Pilomatricoma is a distinctive tumor characterized by a dual population of proliferating basophilic cells and diagnostic shadow cells, believed to arise from the hair matrix. The normal hair matrix undergoes defined cycles of growth (anagen), regression (catagen), and resting (telogen) that are regulated by programmed cell death (apoptosis). bcl-2 is a proto-oncogene that helps to suppress apoptosis in both benign and malignant tumors. In addition, both apoptosis and bel-2 are critical factors in normal hair follicle development. In order to clarify the role of bcl-1, we used immunohistochemical means to study 10 cases of histologically proven pilomatricoma for bcl-2 expression. The study design included both positive and negative controls. All of the pilomatricomas in our series were strongly decorated by bcl-2 immunostaining. Based on our findings of increased bcl-2 staining, we concluded that the faulty suppression of apoptosis contributes to the pathogenesis of pilomatricoma.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9185911&dopt=Abstract
J Dermatol Sci. 1997 May;15(1):36-43.
The promoter of an androgen dependent gene in the hamster flank organ.
Aoki H, Seki T, Sawada J, Handa H, Adachi K.
Life Science Research Laboratories, Shiseido Research Center, Yokohama, Japan.
Hamster flank organs are useful for studying androgen-dependent growth of hair follicles and sebaceous glands. A cDNA clone (FAR-17a) was isolated from the hamster flank organ, whose expression was highly sensitive to androgen. The mRNA level of this gene was reduced after castration but reappeared after testosterone treatment. To elucidate the mechanism of expression of this gene regulated by androgen we isolated a genomic clone, from a hamster genomic library, that includes the promoter and upsteam region. The promoter region was used to drive a luciferase reporter gene in Cos 7 cells. This construct was activated five to six times higher over a control plasmid lacking the promoter region. We tested the effects of testosterone by transfection of the reporter plasmid into androgen dependent SC-3 cells. The results showed up to fivefold stimulation after the addition of androgen. The sequence of this promoter region was analyzed and the transcription factor binding sites were predicted. Since no obvious androgen responsive elements were included in the promoter region, we suggest that the stimulation of the reporter construct has to be mediated indirectly by androgen-dependent transcription factor(s).
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9186810&dopt=Abstract
J Dermatol Sci. 1997 May;15(1):59-63.
Hair follicle dermal papilla cell lines from p53-knockout mice.
Hanzawa C, Kobayashi K, Hirabayashi Y, Inoue T, Aizawa S, Adachi K.
Shiseido Research Center, Yokohama, Japan.
We have attempted to establish a cell line from hair follicle dermal papillae microdissected from vibrissa of mice lacking p53 tumor suppressor gene. The hair follicle dermal papillae were obtained from three types of mice: null knockout, hetero-knockout and wild type litters. Continuous cell lines with short doubling time were obtained only from null knockout litter-mates. Dermal papilla cells from either the hetero-knockout or wild type mice did not multiply well, and died within three passages; provided, however, that in only three cases out of 40 primary dermal papilla implants from two hetero-knockout mice, the cell culture reached 29 passages with a much slower growth rate than the cell lines from the null-knockout mice. These data are in accordance with the notion that the loss of p53 function is closely related to perpetuation of cell cycles and or immortalization.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9186814&dopt=Abstract
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