Literature DB >> 2501035

Epidermal tissue homeostasis: apoptosis and cell emigration as mechanisms of controlled cell deletion in the epidermis of the toad, Bufo bufo.

P E Budtz1, I Spies.   

Abstract

In normal, non-expanding toad epidermis more cells are produced than needed to replace cells lost by moulting. By implication, cell deletion additional to moulting must take place. This paper deals with the mechanisms by which the "surplus" of cells is deleted, taking advantage of the fact that the ratio between cell birth rate (Kb) and the rate of desquamation (Kd), which in normal toads is 2 to 3, can be manipulated. In toads deprived of the pars distalis of the pituitary gland it is decreased to 0.2 to 0.3, and in toads with hydrocortisone pellets implanted into the subcutaneous lymph space it is increased to 7 to 10. Thus, structures candidates for the morphological manifestation of the deletion process should occur rarely in toads in which the pars distalis has been removed and frequently in toads with hydrocortisone pellets implanted. Categorization and enumeration of such structures by light microscopy in the epidermis from operated, normal, and hormone-treated toads were performed. The incidence of structures referred to as "dark cells" and "omega-figures" were found to correlate relatively well with the Kb/Kd-ratio. A subsequent ultrastructural analysis - on a cell-by-cell basis - of "dark cells" showed these to reflect various stages of apoptosis. The duration of the apoptotic process was calculated to be approximately 7 h. Light- and electron microscopy of "omega-figures" combined with histochemical observations of PSA-lectin binding were interpreted as reflecting a release of cells from the basal epidermis and their final elimination within the dermis. It is concluded (i) that apoptosis is an important mechanism of controlled cell deletion, (ii) that emigration to, and elimination in, the dermis is a possible deletion mechanism, and (iii) that necrosis is unlikely to play a role in controlled cell deletion.

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Year:  1989        PMID: 2501035     DOI: 10.1007/bf00225595

Source DB:  PubMed          Journal:  Cell Tissue Res        ISSN: 0302-766X            Impact factor:   5.249


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