Regular ArticlePGE2 Induces c-fos Expression by a cAMP-Independent Mechanism in Glomerular Mesangial Cells
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Inhibitory effects of Aconiti Lateralis Radix Preparata on chronic intermittent cold-induced inflammation in the mouse hypothalamus
2018, Journal of EthnopharmacologyCitation Excerpt :PGE2 is a bioactive lipid derived from arachidonic acid that binds to four cognate G-protein-coupled receptor subtypes (EP1, EP2, EP3 and EP4) and is involved in various aspects of inflammation and immunity (Narumiya, 2007). Moreover, many studies have previously indicated that PGE2 mediates c-Fos activation in fibroblasts, prostate cancer cells, glomerular mesangial cells, and dendritic cells (Chen and Hughes-Fulford, 2000; Danesch et al., 1994; Simonson et al., 1994; Yen et al., 2011). Our data suggest that CIC-induced increase in PGE2 levels in the hypothalamus mediates inflammation and also c-Fos activation, in which ARE treatment attenuated these responses.
Induction of FcγRIIA expression in myeloid PLB cells during differentiation depends on cytosolic phospholipase A<inf>2</inf> activity and is regulated via activation of CREB by PGE<inf>2</inf>
2006, BloodCitation Excerpt :The resolved proteins were electrophoretically transferred to nitrocellulose, which was stained with Ponsue red to detect protein banding, and then blocked in 5% milk in TBS (10 mM Tris,135 mM NaCl, pH 7.4). Immunoblot determination was done as described before27 using primary antibodies against ERK, P-ERK, JNK, P-JNK, p38 MAP kinase, and P-p38 MAP kinase proteins (Santa Cruz Biotechnology), CREB, and P-CREB proteins (Cell Signaling Technology, Beverly, MA) for overnight incubation at 4°C and second antibody, peroxidase conjugated goat antirabbit or antimouse (Amersham Biosciences, Buckinghamshire, United Kingdom) for 1 hour at room temperature and developed using the enhanced chemiluminescence (ECL) detection system (Amersham Biosciences). For immunoblot detection of CREB, the nuclei fractions of 2 × 106 cells were immediately solubilized in electrophoresis sample buffer and processed for separation on 10% SDS-polyacrylamide gel electrophoresis (SDS-PAGE).
Cyclooxygenase-2 Inhibitor (SC-236) Suppresses Activator Protein-1 through c-Jun NH2-Terminal Kinase
2004, GastroenterologyCitation Excerpt :These results indicated that the inhibitory effect on AP-1 and JNK activation was not necessarily related to the inhibition of COX-2 enzyme activity and was not universal for all COX-2 inhibitors. Several studies have suggested that PGE2 promoted tumorigenesis through the activation of AP-1.45–47 Consequently, we considered the possibility that inhibition of COX-2-prostaglandins synthesis executed autoregulatory effect on AP-1 activity and cell growth.
NS-398 and piroxicam suppress UVB-induced activator protein 1 activity by mechanisms independent of cyclooxygenase-2
2003, Journal of Biological ChemistryCitation Excerpt :COX inhibitors block the catalysis of arachidonic acid to PGE2 (39–41). Several studies suggest that PGE2 signals through AP-1 and, thus, may play a definitive role in tumor development (42–44). To elucidate whether NS-389 or piroxicam blocks AP-1 activation by attenuating PGE2production, we transfected two acetylation active site mutants of COX-2, S516 M and S516Q, together with the AP-1 luciferase reporter gene into Cox-2−/− cells.