gw-1929 and 2-2-bis(4-glycidyloxyphenyl)propane

gw-1929 has been researched along with 2-2-bis(4-glycidyloxyphenyl)propane* in 1 studies

Other Studies

1 other study(ies) available for gw-1929 and 2-2-bis(4-glycidyloxyphenyl)propane

Article	Year
PPARgamma agonists inhibit angiogenesis by suppressing PKCalpha- and CREB-mediated COX-2 expression in the human endothelium. Cardiovascular research, 2010, May-01, Volume: 86, Issue:2 The activation of peroxisome proliferator-activated receptor (PPAR)gamma is known to inhibit angiogenesis. As a potential mechanism for this, we aimed at examining the effects of PPARgamma agonists on the pro-angiogenic enzyme cyclooxygenase (COX)-2 in human endothelium.. Cultured endothelial cells were pre-incubated with the PPARgamma agonists rosiglitazone (RSG) or GW1929 before stimulation with vascular endothelial growth factor (VEGF) or phorbol myristate acetate (PMA). RSG and GW1929 attenuated VEGF- and PMA-stimulated COX-2 activity, as well as protein and mRNA expression. This effect was abolished by the PPARgamma antagonists bisphenol A diglycidyl ether and GW9662 as well as by PPARgamma small-interfering RNAs (siRNAs). Transient transfection experiments revealed that the induction of COX-2 promoter was significantly inhibited by RSG through an interference with the cAMP response element (CRE) site. COX-2 downregulation after siRNA targeting CRE-binding protein (CREB) confirmed the role of CREB in mediating COX-2 transcription. Correspondingly, PPARgamma agonists attenuated CREB activation. As both protein kinase C (PKC)alpha and beta are involved in VEGF-induced COX-2 expression and CREB activation, we investigated which isoform(s) of PKC was affected by RSG. RSG only reduced VEGF- and PMA-stimulated PKCalpha membrane translocation.. VEGF induces CREB-mediated COX-2 expression through a PKCalpha-dependent pathway in human endothelium. The anti-angiogenic effect of PPARgamma agonists is due, at least in part, to an interference with the VEGF-stimulated PKCalpha-mediated activation of CREB and the related expression of COX-2. Topics: Angiogenesis Inhibitors; Anilides; Benzhydryl Compounds; Benzophenones; Binding Sites; Cells, Cultured; Cyclic AMP Response Element-Binding Protein; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Down-Regulation; Endothelial Cells; Epoxy Compounds; Gene Expression Regulation, Enzymologic; Humans; Neovascularization, Physiologic; Nitrobenzenes; PPAR gamma; Promoter Regions, Genetic; Protein Kinase C-alpha; Protein Transport; RNA Interference; RNA, Messenger; Rosiglitazone; Sulfonamides; Tetradecanoylphorbol Acetate; Thiazolidinediones; Transfection; Tyrosine; Vascular Endothelial Growth Factor A	2010

Article

Year

PPARgamma agonists inhibit angiogenesis by suppressing PKCalpha- and CREB-mediated COX-2 expression in the human endothelium.

Cardiovascular research, 2010, May-01, Volume: 86, Issue:2

The activation of peroxisome proliferator-activated receptor (PPAR)gamma is known to inhibit angiogenesis. As a potential mechanism for this, we aimed at examining the effects of PPARgamma agonists on the pro-angiogenic enzyme cyclooxygenase (COX)-2 in human endothelium.. Cultured endothelial cells were pre-incubated with the PPARgamma agonists rosiglitazone (RSG) or GW1929 before stimulation with vascular endothelial growth factor (VEGF) or phorbol myristate acetate (PMA). RSG and GW1929 attenuated VEGF- and PMA-stimulated COX-2 activity, as well as protein and mRNA expression. This effect was abolished by the PPARgamma antagonists bisphenol A diglycidyl ether and GW9662 as well as by PPARgamma small-interfering RNAs (siRNAs). Transient transfection experiments revealed that the induction of COX-2 promoter was significantly inhibited by RSG through an interference with the cAMP response element (CRE) site. COX-2 downregulation after siRNA targeting CRE-binding protein (CREB) confirmed the role of CREB in mediating COX-2 transcription. Correspondingly, PPARgamma agonists attenuated CREB activation. As both protein kinase C (PKC)alpha and beta are involved in VEGF-induced COX-2 expression and CREB activation, we investigated which isoform(s) of PKC was affected by RSG. RSG only reduced VEGF- and PMA-stimulated PKCalpha membrane translocation.. VEGF induces CREB-mediated COX-2 expression through a PKCalpha-dependent pathway in human endothelium. The anti-angiogenic effect of PPARgamma agonists is due, at least in part, to an interference with the VEGF-stimulated PKCalpha-mediated activation of CREB and the related expression of COX-2.

Topics: Angiogenesis Inhibitors; Anilides; Benzhydryl Compounds; Benzophenones; Binding Sites; Cells, Cultured; Cyclic AMP Response Element-Binding Protein; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Down-Regulation; Endothelial Cells; Epoxy Compounds; Gene Expression Regulation, Enzymologic; Humans; Neovascularization, Physiologic; Nitrobenzenes; PPAR gamma; Promoter Regions, Genetic; Protein Kinase C-alpha; Protein Transport; RNA Interference; RNA, Messenger; Rosiglitazone; Sulfonamides; Tetradecanoylphorbol Acetate; Thiazolidinediones; Transfection; Tyrosine; Vascular Endothelial Growth Factor A

2010