Journal
JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 81, Issue 3, Pages 168-174Publisher
SPRINGER-VERLAG
DOI: 10.1007/s00109-003-0418-y
Keywords
glucocorticoid receptor; nontranscriptional; nitric oxide; ischemia; Akt
Funding
- NHLBI NIH HHS [R01 HL052233-07, R01 HL070274-02, P01 HL048743-120008, R01 HL052233-06, R01 HL070274, R01 HL052233, R01 HL070274-01, R01 HL052233-05, P01 HL048743] Funding Source: Medline
- NIDDK NIH HHS [R01 DK062729-01A1, R01 DK062729] Funding Source: Medline
- NINDS NIH HHS [P01 NS010828-330036, P50 NS010828, P50 NS010828-290036, P01 NS010828] Funding Source: Medline
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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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