Inactivation of CES1 Blocks Prostaglandin D₂ Glyceryl Ester Catabolism in Monocytes/Macrophages and Enhances Its Anti-inflammatory Effects, Whereas the Pro-inflammatory Effects of Prostaglandin E₂ Glyceryl Ester Are Attenuated.

ABSTRACT: Human monocytic cells in blood have important roles in host defense and express the enzyme carboxylesterase 1 (CES1). This metabolic serine hydrolase plays a critical role in the metabolism of many molecules, including lipid mediators called prostaglandin glyceryl esters (PG-Gs), which are formed during cyclooxygenase-mediated oxygenation of the endocannabinoid 2-arachidonoylglycerol. Some PG-Gs have been shown to exhibit anti-inflammatory effects; however, they are unstable compounds, and their hydrolytic breakdown generates pro-inflammatory prostaglandins. We hypothesized that by blocking the ability of CES1 to hydrolyze PG-Gs in monocytes/macrophages, the beneficial effects of anti-inflammatory prostaglandin D₂-glyceryl ester (PGD₂-G) could be augmented. The goals

SUBMITTER: Scheaffer HL 

PROVIDER: S-EPMC7675540 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature