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October 1982

Psoriasis as a Possible Defect of the Adenyl Cyclase-Cyclic AMP Cascade: A Defective Chalone Mechanism?

Author Affiliations

Ann Arbor, Mich

From the Department of Dermatology, University of Michigan Medical School, Ann Arbor.

Arch Dermatol. 1982;118(10):862-868. doi:10.1001/archderm.1982.01650220166025

Epidermal cell division appears to be slowed by beta adrenergic stimulation. The satisfaction of Sutherland's four criteria of an adenosine 3′, 5′ = monophosphate (cyclic AMP) mediated event shows that the inhibition is due to an increase intraepidermal cyclic AMP. Since increasing cyclic AMP slows epidermal cell division and mediates glycogen breakdown, we suggest that psoriasis may be a polygenic-environmentally induced defect in the adenyl cyclase-cyclic AMP cascade. Such a defect could explain that seemingly paradoxical occurrence of the 12-fold acceleration in the rate of cell division, low phosphorylase activity, and glycogen buildup in the epidermis of a psoriatic lesion. Our approach to the detection of a possibly defective adenyl cyclase-cyclic AMP-cyclic AMP dependent protein kinase cascade and how such a defect, if it is found, might be corrected by therapy is discussed.

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