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  • 1985-1989  (4)
  • 1
    ISSN: 1365-2133
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Two monoclonal antibodies which reacted with the epidermal cell surface (SF-1) and the dermal-epidermal-junction (SF-2), respectively, were obtained by immunizing mice with partially-purified human epibolin. The corresponding antigens were partially purified from fetal bovine serum by affinity chromatography using these antibodies. SDS-polyacrylamide gel electrophoresis showed that these antigens contained polypeptide components with molecular weights different from that of epibolin (mol. wt. 65000 daltons); SF-1 antigen had a 68000 dalton main component, and SF-2 antigen a broad 58000–61000 dalton main component. Both of these partially-purified antigens promoted the spreading of dissociated pig epidermal cells. SF-2 antigen also promoted the spreading of Pam cells (a murine keratinocyte line). The results suggest that proteins capable of promoting epidermal cell spreading may be present on the epidermal cell surface and at the dermal-epidermal junction. However, their physiological role in keratinization remains to be elucidated.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Archives of dermatological research 279 (1987), S. 530-535 
    ISSN: 1432-069X
    Schlagwort(e): Adenylate cyclase ; Cell culture ; Trichilemmoma
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The adenylate cyclase system of an established human trichilemmoma cell line was investigated. Stimulators of human epidermal adenylate cyclase system, epinephrine, histamine, adenosine, and prostaglandin E increased cyclic AMP levels of the trichilemmoma cells. The effects of epinephrine, histamine, and adenosine were inhibited by the addition of propranolol (a beta-adrenergic antagonist), cimetidine (histamine H2-antagonist), and theophylline (adenosinereceptor antagonist), respectively. The epinephrine, histamine, and protaglandin E effects were augmented by the addition of cyclic AMP (cAMP) phosphodiesterase inhibitor, isobutylmethylxanthine (IBMX); the adenosine effect was augmented by another phosphodiesterase inhibitor, papaverine. Without the addition of these phosphodiesterase inhibitors, the maximal accumulations were observed at 3 min incubation. Following this, the cAMP content returned to the basal level, and the cells did not respond to repeated stimulations with the same initial stimulator. This fact indicates receptor-specific refractoriness. For example, epinephrine-pretreated cells did not respond to epinephrine, but retained their sensitivity to histamine. It has been known that normal epidermal keratinocytes are regulated in vitro by glucocorticoids, colchicine, and retinoids, resulting in the augmentation of their beta-adrenergic response. Only hydrocortisone treatment on the trichilemmoma cells resulted in the augmentation of the beta-adrenergic response. Although the established human trichilemmoma cell line has similar adenylate cyclase systems as normal epidermis, it apparently has lost some of the regulatory mechanism of the beta-adrenergic response.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-069X
    Schlagwort(e): Epidermis ; Adenylate cyclase ; Cyclic AMP ; UVB ; Oxygen intermediates ; Superoxide dismutase
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary UVB irradiation augmented the betaadrenergic adenylate cyclase response of pig skin epidermis in vitro. The effect was observed 2–4 h following the irradiation and lasted at least for 48 h. There was no significant difference in cyclic AMP phosphodiesterase activity between control and UVB-irradiated epidermis at lower irradiation dose (150 mJ/cm2), which is the dose of the most marked beta-adrenergic augmentation effect. The augmentation effect was specific to the beta-adrenergic system; adenosine and histamine adenylate cyclase responses were unchanged or decreased depending on the irradiation dose. Histologically, marked sumburn-cell formation was observed following the UVB irradiation. It has been suggested that oxygen intermediates generated by ultraviolet radiation participate in sunburncell formation. The addition of superoxide dismutase (SOD) in the incubation medium significantly inhibited sunburn-cell formation. On the other hand, the beta-adrenergic augmentation effect was not affected by the addition of SOD. Other scavengers of oxygen intermediates (catalase, catalase+SOD, xanthine, or mannitol) did not inhibit the UVB-induced beta-adrenergic augmentation effect. Further, superoxide-anion generating systems (hypoxanthine-xanthine oxidase system and acetaldehyde-xanthine oxidase system) revealed no stimulatory effect on the beta-adrenergic response of epidermis. These results indicate that (a) the UVB-induced beta-adrenergic augmentation effect is inherent to skin and does not depend on systemic factors such as inflammatory infiltrates following UVB irradiation; (b) in contrast to sunburn-cell formation, induction of the beta-adrenergic adenylate cyclase response is not directly associated with oxygen intermediates generated by UVB irradiation.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    ISSN: 1432-069X
    Schlagwort(e): β-Adrenergic receptor ; Monoclonal antibody
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary We have developed two types of hybridomas producing monoclonal antibodies to the turkey erythrocyte β1-adrenergic receptor in order to study the β-adrenergic-cAMP system of epidermis. Splenic cells from BALB/c mice immunized with partially purified turkey erythrocyte β1-adrenergic were fused with mouse myeloma cell line SP2/0-Ag14. Five hybridomas of 17 positive cells producing antibodies which could precipitate soluble turkey erythrocyte β1-receptors were cloned by the limiting dilution method. The antibodies cross-reacted with β- and β2-adrenergic receptors and stained epidermal basal cells with immunocytochemical techniques. Neither type of antibody interfered with the antagonist binding, i.e., all antibodies bound to sites other than the ligand binding site on the surface. One type of antibody inhibited epinephrine-stimulated adenylate cyclase activity in our “leaky” epidermal cell system. The data suggest that the antibody interferes with the coupling of the receptor to the regulatory protein.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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