PGE2, synthesis

Han M, Wen JK, Zheng B, Zhang DQ. Acetylbritannilatone suppresses NO and PGE2 synthesis in RAW 264.7 macrophages through the inhibition of iNOS and COX-2 gene expression. Life Sci 2004 75 675-684. 

The proinflammatory cytokines (interleukins 1 and 6 and tumour necrosis factor alpha) from macrophages are raised in depression. This leads to increased PGE2 synthesis and release which may lead to a reduction in central monoamine release. 

Liu, K-L. and Belury, M.A., Conjugated linoleic acid reduces arachidonic acid content and PGE2 synthesis in murine keratinocytes, Cancer Lett., 1 A, 1050, 1998. 

Analgesic Decreased PGE2 synthesis PGE2 normally sensitises nerves to histamine and bradykinin. 

Antipyretic Decreased PGE2 synthesis PGE2 normally elevates the set-point of the hypothalamic thermoregulator, and is normally elevated during infection or inflammation. 

The current theory of the mechanism relates to the inhibition of cyclo-oxygenases (79) and a greater degree of interference with PGE2 synthesis, allowing the bronchoconstrictor PGF2 to predominate in susceptible individuals. 

L.J. Murphey, M.K. Williams, S.C. Sanchez, L.M. Byrne, I. Csiki, J.A. Oates, D.H. Johnson, J.D. Morrowa, Quantification of the major urinary metabolite of PGE2 by a LC-MS assay determination of cyclooxygenase-specific PGE2 synthesis in healthy humans and those with lung cancer. Anal. Biochem., 334 (2004) 266. 

Endothelium PGE2, synthesis adhesion molecule expression... 

Fluid and electrolyte loss in cholera patients is closely related to elevated concentrations of cAMP, which can stimulate chloride secretion in intestinal epithelial cells (Field, 1971 Moss and Vaughan, 1988a). There is also evidence for the importance of other substances, such as prostaglandin E2 (PGE2) and 5-hydroxytryptamine (5-HT), in CT-induced secretion (Kaper et al., 1995). Nilsson et al. (1983) reported that 5-HT was released from enterochromaffin cells in the cat small intestine upon CT treatment. 5-HT could then stimulate PGE2 synthesis (Beubler etai, 1989) and activate the enteric nervous system (Ekiund et al., 1984). Cholera toxin also caused release of PGE2 into the lumen of intestinal loops in vitro (Peterson and Ochoa, 1989), via an effect on arachidonic acid formation (Peterson et al., 1990 Reit-meyer and Peterson, 1990). The contribution of these, and perhaps other, CT effects to the pathogenesis of cholera remains to be elucidated (Peterson etai, 1994). 

However, the mechanism by which minute changes in extracellular calcium could have major effects on blood pressure regulation and, consequently, on the development of primary hypertension, has not yet been fully elucidated. There is preliminary evidence that activation of the renal CaR leads to enhanced prostaglandin E2 (PGE2) synthesis, with natriuresis as a consequence. The concomitant reduction in plasma volume would then account for the blood pressure-lowering effect of elevated extracellular calcium (Wang et al. 2001). 

PGE can stimulate or inhibit its own hormone-induced synthesis via an ability to stimulate cAMP production. In the canine renal collecting tubule there appear to be two PGE receptors ". One of these receptors is an inhibitory receptor which modulates vasopressin-induced H2O flow . The other receptor is coupled to stimulation of adenylate cyclase activity. This latter receptor may be involved in inhibition of arachidonate release and feedback inhibition of hormone-induced PGE production. Similarly, neutrophil activation (and PGE2 synthesis) induced by f-met-leu-phe is under feedback inhibitory control by a PGE receptor apparently coupled to The opposite situation occurs in the thyroid. In the thyroid, there are two phases to PGE synthesis. The second phase is cAMP dependent and PGE serves to augment its own synthesis by its ability to stimulate adenylate cyclase activity ... 

Ma D.W., C.J. Field, M.T. Clandinin. An Enriched Mixture of trans- 10,cm-12-CLA Inhibits Linoleic Acid Metabolism and PGE2 Synthesis in MDA-MB-231 Cells. Nutr. Cancer 44(2) 203-12 (2002). 

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