Evidence is provided for a possible dermal influence on the epidermis. Topical vitamin A stimulates a number of dermal cells with different enzyme reactions, and these invade the epidermis at about the time a granular layer is induced in mouse tail scale epidermis. N-hexadecane also induced a granular layer formation in the tail scale epidermis but the application of this agent only results in the invasion of the epidermis by non-specific esterase cells. These non-specific esterase cells are present in the follicular zone where a granular layer is usually present. It appears that dendritic cells may be responsible for the formation of a granular layer and that these cells in some way influence the keratinocytes to discharge their lyosomal enzymes and thus form a granular layer. It appears unlikely that the dendritic cells actually contribute their own acid hydrolases to the cell cytolysis necessary for the production of granular layer.
This article describes a new animal model for the evaluation of drugs that may prevent the development of parakeratosis. The advantages of this model are simplicity, economy, and the opportunity to observe the possible occurrence of acute systemic toxic reactions. High-boiling coal tar acids (phenols), vitamin A (retinyl acetate), and hydrocortisone butyrate (Locoid) were assayed. Only tar phenols consistently prevented scale development. Vitamin A was not properly screened because of toxic effects that resulted in premature termination of the experiment.
Over the lint week of postnatal life, dermal dendritic cells stream upwards to invade the epidermis of the mouse tail and back skin. Their migrations seem associated with the development of distinct types of epidermal physiology:ortho‐ and parakeratosis. Changes from neonatal epidermal morphology occur at similar times in both back and tail skin. The hairv mouse back skin is alwavs orthokeratotic, but the initially orthokeratotic tail epidermis later becomes parakeratolir in the scale regions, remaining orthokeratotic in areas of hair production.
Dermal cells studied were adenosine triphosphatase (ATPase)‐, non‐specific esterase (NSE)‐, naphthvl AS‐D chloroacetate‐, and dihydroxyphenvlalanine (dopa)‐positive dendritic cells. The results are discussed in connection with hair growth and glabrous epidermal kcratinization. Dendritic cell regulation of epidermal physiology involving the dermis and pilosebaceous unit is discussed in relation to reviewed work on mesenchymal‐epithelial interactions in animal and human skin.
Summary
The induced enzyme activity in epidermal cells following the topical application of retinyl acetate has been investigated. It has been shown that within 2 days there is a reaction for alkaline phosphatase and phosphodiesterases using thymidine‐5‐monophosphate and cyclic 3′5′‐adenosine monophosphate as substrates. These reactions increase up to the 4th day and then become weaker. At about the 6th day a granular layer is induced in the tail scale region where none previously existed. There is evidence that the reaction returns between the 18th and 20th days. It is thought that the 3′5′‐cyclic AMP phospho‐diesterase reduced the c̄AMP content of epidermal cells and thus allows epidermal proliferation as shown by increased thickness of the epidermis and increased mitotic activity. The complex interactions of c̄AMP and c̄GMP phosphodiesterases and the periodic variations of the induced enzyme activity within the epidermal cells are discussed.
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