| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1986: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1985: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1984: ¥700,000 (Direct Cost: ¥700,000)
|
|---|
| 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.
|
