August 20, 2008Open Access

Glucocorticoid response elements and 11β-hydroxysteroid dehydrogenases in the regulation of endothelial nitric oxide synthase expression

Key Points

Key points are not available for this paper at this time.

Abstract

We identified the first GRE in the eNOS promoter region and demonstrated that endogenous 11 beta-HSD1 and 11 beta-HSD2 play significant and distinct roles in modulating the effect of glucocorticoids on eNOS expression.

Read Full Paperexternally

Bookmark

View Full Paper

Cite This Study

Liu et al. (Wed,) studied this question.

synapsesocial.com/papers/69d850bd33ca018b39ae38cb https://doi.org/https://doi.org/10.1093/cvr/cvn231

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Mechanisms of glucocorticoid signalling2004 · 311 citations
2Diagnosis of Cushing’s syndrome: Re-evaluation of midnight plasma cortisol vs urinary free cortisol and low-dose dexamethasone suppression test in a large patient group1999 · 66 citations
3Negative Glucocorticoid Receptor Response Elements and their Role in Glucocorticoid Action2004 · 219 citations
4Flow- and bradykinin-induced nitric oxide production by endothelial cells is independent of membrane potential1996 · 20 citations
5Suppression of 11β-hydroxysteroid dehydrogenase type 1 with RNA interference substantially attenuates 3T3-L1 adipogenesis2007 · 30 citations

Bookmark

View Full Paper