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October 1982

Commentary: Cyclic Adenosine Monophosphate Regulation of Normal and Psoriatic Epidermis

Author Affiliations

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

Arch Dermatol. 1982;118(10):869-874. doi:10.1001/archderm.1982.01650220173026

An article previously published in the Archives1 proposed decreased activity in the cyclic adenosine monophosphate (cAMP) cascade as one potential molecular explanation of the following three characteristics of lesional epidermis in psoriasis: (1) increased cellular proliferation, (2) increased glycogen, and (3) decreased cellular differentiation. In nonepidermal cells, cAMP was known to decrease proliferation, decrease glycogen, and increase differentiation. The cAMP hypothesis assumed that, at the level of molecular regulation, epidermal and nonepidermal cells would be similar rather than dissimilar. If so, decreased cascade activity in different epidermal layers would be one explanation for three lesional characteristics.

EPIDERMAL HOMEOSTASIS  If the cAMP hypothesis is a tenable explanation for misregulated epidermal proliferation in psoriasis, it must be compatible with our current understanding of proliferative homeostasis. This is the mechanism used to maintain low-level cell proliferation that is sufficient to provide new cells to replace those sloughed from the surface of relatively

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