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October 1971

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. 1971;104(4):352-358. doi:10.1001/archderm.1971.04000220010003

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 intra-epidermal 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.