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Intensive Care Medicine Experimental
Fig. 1 | Intensive Care Medicine Experimental

Fig. 1

From: Increased glucocorticoid receptor expression in sepsis is related to heat shock proteins, cytokines, and cortisol and is associated with increased mortality

Fig. 1

Glucocorticoids (GC) diffuse across the cell membrane and bind to human glucocorticoid receptor (hGR) in the cytoplasm. In a heat shock protein (HSP) heterocomplex, hGRα is activated (upon ligand binding), is released from HSP72 and HSP90α, and rapidly translocates into the nucleus, where the transcription of target genes is initiated. Through transactivation, binding of two hGRα molecules together as a homodimer to glucocorticosteroid response elements (GRE) in the promoter region of steroid-sensitive genes leads to the transcription of genes encoding anti-inflammatory mediators (i.e., IL-10) and the inhibition of nuclear factor-κB (NF-κB). Through transrepression, the hGRα–GC complex interacts with the activated by NF-κB and other pro-inflammatory transcription factors with intrinsic histone acetyltransferase (HAT) activity switching off multiple activated inflammatory genes (i.e., IL-6). CBP cAMP response element binding protein, IKKβ inhibitor of I-κB kinase-β

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