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Nontranscriptional actions of the glucocorticoid receptor

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Abstract

Many cellular responses to corticosteroids involve the transcriptional modulation of target genes by a prototypical nuclear receptor, the glucocorticoid receptor (GR). In the classic model of steroid hormone action GR acts as ligand-dependent transcription factor by either activating or repressing gene expression through direct interactions with DNA or other transcription factors. Recent evidence suggests an important role for nontranscriptional effects of GR in the vascular system. The nontranscriptional actions of GR involve the rapid activation of protein kinases, such as phosphatidylinositol-3 kinase and Akt, leading to the activation of endothelial nitric oxide synthase. This novel pathway of steroid hormone action protects against ischemic injury by augmenting blood flow and decreasing vascular inflammation.

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Abbreviations

AP :

Activator protein

DBD :

DNA-binding domain

Dex :

Dexamethasone

eNOS :

Endothelial nitric oxide synthase

ER :

Estrogen receptor

GR :

Glucocorticoid receptor

GRE :

Glucocorticoid response elements

JNK :

Jun N-terminal kinase

LBD :

Ligand-binding domain

NF-κB :

Nuclear transcription factor κB

PI3K :

Phosphatidylinositol 3-kinase

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  1. Vascular Medicine Research, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 65 Landsdowne Street, Cambridge, MA 02139, USA

    Florian P. Limbourg & James K. Liao

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Limbourg, F.P., Liao, J.K. Nontranscriptional actions of the glucocorticoid receptor. J Mol Med 81, 168–174 (2003). https://doi.org/10.1007/s00109-003-0418-y

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