Abstract

Apoptosis, a physiological cell death, has been shown to be involved in tissue homeostasis as well as in tissue regression due to hormone deprivation. The thyroid cell population slowly turns over, with cell loss compensating mitogenicity. In the absence of thyrotropin, the cell population decreases. The possible involvement of apoptosis in this loss has been studied. We show in this report that deprivation of serum, epidermal growth factor and thyrotropin triggers internucleosomal DNA fragmentation and morphological modifications characteristic of apoptotic cell death in dog thyroid cells in primary culture; cycloheximide treatment has the same effect. This indicates that thyrocytes are endowed with a constitutive apoptosis "program" and that the latter might be involved in the thyroid regression observed in vivo in the absence of full growth stimulation of the gland.

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