Thioredoxin in the endocrine response to stress.

摘要: Adaptation to stress evokes a variety of biological responses, including activation the hypothalamic–pituitary–adrenal (HPA) axis and synthesis panel stress-response proteins at cellular levels: for example, expression thioredoxin (TRX) is significantly induced under oxidative conditions. Glucocorticoids, as peripheral effector HPA axis, exert their action via interaction with ligand-inducible transcription factor glucocorticoid receptor (GR). However, how these responses coordinately regulate metabolism still unknown. We demonstrate that either antisense TRX or treatment H 2 O negatively modulates GR function decreases glucocorticoid-inducible gene expression. Impaired response glucocorticoids rescued by overexpression TRX, most probably through functional replenishment GR. Moreover, not only ligand binding domain but DNA also suggested be direct target TRX. Together, we propose responsiveness modulated redox state level, suggesting cross-talk between neuroendocrine control antioxidant systems may essential mammalian adaptation processes.