1986 Fiscal Year Final Research Report Summary
Regulatory system of epidermal adenylate cyclase-cyclic AMP system
| Project/Area Number |
59570413
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Hokkaido University (1986)
Asahikawa Medical College (1984-1985) |
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Principal Investigator |
OHKAWARA Akira Hokkaido University School of Medicine, Professor, 医学部, 教授 (50000964)
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| Project Period (FY) |
1984 – 1986
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| Keywords | cyclic AMP / adenylate cyclase / glucocorticoid / colchicine / retinoid / 尋常性乾癬 |
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| Research Abstract |
Glucocorticoid ( hydrocortisone ) augmented the beta-adrenergic adenylate cyclase response of epidermis. The effect was observed by other glucocorticoids ( prednisolone and dexamethasone ) but not androgens or estrogens. Potent glucocorticoids revealed the beta-adrenergic augmentation effect at lower concentrations. Protein synthesis inhibitors ( actinomycin D, cycloheximide and puromycin ) inhibited the beta-adrenergic augmentation effect by the glucocorticoid. These compounds, however, revealed the beta-adrenergic augmentation effect when added singly to the incubation medium at a restricted range of concentrations. Besides glucocorticoids, microtubules disruptive agent ( colchicine ) and retinoids ( retinoic acid, RO 10-1670, E-5166 ) revealed the beta-adrenergic augmentation effect. The effect by these 3 types of chemicals were apparently independent each other. Psoriatic involved epidermis has been characterized by a defective beta-adrenergic adenylate cyclase response of epidermis. Although many antipsoriatic agents, which include glucocorticoids,colchicine and retinoids, revealed the beta-adrenergic augmentation effect, the significance of these findings in terms of the regulatory system of keratinocyte proliferation remains unknown at present.
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