Biochemical and Biophysical Research Communications
Regular ArticleGlucocorticoid-Mediated Suppression of the Promoter Activity of the Cyclooxygenase-2 Gene Is Modulated by Expression of Its Receptor in Vascular Endothelial Cells☆
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Glucocorticoids and estrogens modulate the NF-κB pathway differently in the micro- and macrovasculature
2013, Medical HypothesesCitation Excerpt :Recent observations indicate that glucocorticoid receptors in the macrovasculature can repress the gene transcription of these inflammatory molecules by interaction with transcription factor such as NF-κB [10]. In addition, glucocorticoids inhibit the expression of COX-2 in ECs stimulated with pro-inflammatory cytokines and LPS [25]. Several studies have demonstrated that glucocorticoids reduce the expression of eNOS and iNOS and consequently the production of NO in human endothelial cells [39].
Endothelial cells are a potential site of interaction between estrogens and glucocorticoids
2009, Bioscience HypothesesCitation Excerpt :Recent observations indicate that glucocorticoid receptors in the macrovasculature can repress the gene transcription of these inflammatory molecules by interaction with transcription factors such as AP-1 and NF-kappaB [49]. In addition, glucocorticoids inhibit the expression of COX-2 in endothelial cells stimulated with pro-inflammatory cytokines and LPS [50]. Several studies have demonstrated that glucocorticoids reduce the expression of eNOS and iNOS and consequently the production of NO in human endothelial cells [51].
p38 MAPK mediates COX-2 gene expression by corticosterone in cardiomyocytes
2008, Cellular SignallingSulforaphane suppresses lipopolysaccharide-induced cyclooxygenase-2 (COX-2) expression through the modulation of multiple targets in COX-2 gene promoter
2007, International ImmunopharmacologyCitation Excerpt :These findings suggest that the inhibitory effects of sulforaphane on the LPS-induced COX-2 gene expression are due to the suppression of COX-2 mRNA expression. The COX-2 promoter region (− 327/+ 59) contains 3 cis-acting elements, namely, NF-κB binding site, C/EBP binding site, and CREB binding site, all of which have been shown to be involved in the regulation of COX-2 gene transcription [15,16,18]. To identify which cis-acting elements play a critical role in sulforaphane-mediated COX-2 promoter inhibition, mutants of the three cis-acting elements were tested in transfection assay (Fig. 1D).
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Abbreviations used: PG, prostaglandin; COX, Cyclooxygenase; LPS, lipopolysaccharide; DEX, dexamethasone; BAEC, bovine arterial endothelial cells; GR, glucocorticoid receptor; TPA, 12-O-tetradecanoyl phorbol-13-acetate; CRE, cyclic AMP response element; NF-IL6, nuclear factor for interleukin-6 expression; NF-κB, nuclear factor κB; C/EBP, CCAAT/enhancer binding protein; CREB, CRE binding protein; CBP, CREB binding protein; GAPDH, glyceraldehyde-3-phosphate dehydrogenase
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