Regulation of Apoptosis via Steroid Receptors
Steroid hormones play essential roles in a variety of physiological processes including embryonic development, sexual differentiation and maturation, and metamorphosis. The homeostatic regulation of metabolism and cell turnover that determines tissue sizes and shapes are also under the influence of these hormones. Apoptosis is involved in many of these phenomena, The pharmacological or surgical manipulation of animals to change steroid levels often causes involution or enlargement of certain tissues partly through the enhancement or inhibition of apoptosis. For example, an elevation of blood glucocorticoid level, by an injection of glucocorticoids or by excessive stress, causes thymus involution due to apoptosis in cortical immature thymocytes (Claman 1972). By contrast, adrenalectomy of mice causes not only depletion of glucocorticoids from the plasma but also a marked increase in the thymus size (Shortman and Jackson 1974). Glucocorticoid-induced apoptosis is dependent on the binding of glucocorticoids to glucocorticoid hormone receptors (GRs), which is also required in the general effects of steroids (Duval et al. 1984). The steroid receptors such as GR, mineralcorticoid receptors, progesterone receptors, androgen receptors, and estrogen receptors are members of a superfamily of ligand-inducible transcription factors. The steroid receptor superfamily also includes retinoic acid receptors, thyroid hormone receptors, vitamin D3 receptors, ecdysone receptors, and COUP transcription factor. They are related to v-erbA oncogene.
KeywordsRetinoic Acid Okadaic Acid Palatal Shelf Thymic Selection Thymocyte Apoptosis
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