c-Jun N-terminal Kinase-mediated Stabilization of Microsomal Prostaglandin E2 Synthase-1 mRNA Regulates Delayed Microsomal Prostaglandin E2 Synthase-1 Expression and Prostaglandin E2 Biosynthesis by Cardiomyocytes

Abstract

Microsomal prostaglandin (PG)Ecan participate in the regulation of mPGES-1 protein synthesis in these cells, and that mPGES-1 catalyzes the majority of LPS-induced PGE 2 biosynthesis by cardiomyocytes.

Microparticles stimulate the synthesis of prostaglandin E2 via induction of cyclooxygenase 2 and microsomal prostaglandin E synthase 1

“…Our findings on the roles of NF-B and AP-1 in the induction of mPGES-1 by microparticles support those of other studies in the setting of cytokine-mediated up-regulation of mPGES-1. Thus, in cardiomyocytes, interleukin-1 stimulates the expression of mPGES-1 mRNA, an effect abrogated by pretreatment with the JNK inhibitor SP600125 (31). Other evidence for a role of NF-B in the induction of mPGES-1 comes from studies with curcumin, an agent that prevents the degradation of IB and thereby inhibits NF-B signaling.…”

Lack of Microsomal Prostaglandin E 2 Synthase-1 in Bone Marrow–Derived Myeloid Cells Impairs Left Ventricular Function and Increases Mortality After Acute Myocardial Infarction

“…Construction of the mPGES-1-deficient mouse line (Ptges Ϫ/Ϫ , DBA/1lacJ background), 13 real-time quantitative polymerase chain reaction studies, 2-dimensional echocardiography, invasive hemodynamic assessment of LV function, morphometric assessment of hearts that were perfusion fixed at an intraventricular pressure of 20 mm Hg in situ, liquid chromatography-tandem mass spectrometry-based evaluation of prostanoid levels in cardiac tissue, immunoblotting, and lectin and Picrosirius Red staining were performed exactly as described previously. 9,12,14 Housing and experimental procedures were approved by the Animal Care Committee of the University Health Network and were in accordance with the Guide for the Care and Use of Laboratory Animals research statutes, Ontario (1980).…”

“…mPGES-1 is encoded by the Ptges gene and can be expressed by leukocytes, 7 cardiac fibroblasts, 8 and cardiac myocytes. 9 Inhibition of the PGE 2 receptor EP4 attenuates cardiomyocyte hypertrophy in vitro, 10 and deletion of EP4 exacerbates myocardial ischemia/reperfusion injury in vivo. 11 In addition, Ptges Ϫ/Ϫ mice develop more LV dilation, worse LV contractile function, and higher LV end-diastolic pressure than Ptges ϩ/ϩ mice after MI.…”

Variants of gene for microsomal prostaglandin E2 synthase show association with disease and severe inflammation in rheumatoid arthritis

“…3¢UTR is involved in post-transcriptional gene regulation via mRNA stability, the mechanism for which is revealed in the regulation of mouse Ptges gene expression. 36 These SNPs may be regulatory or in linkage disequilibrium with other regulatory polymorphisms in 3¢UTR that could similarly modulate the human mPGES-1 expression and predispose individuals to RA.…”