Lipopolysaccharide-induced inflammation in human peritoneal mesothelial cells is controlled by ERK1/2-CDK5-PPARγ axis

Abstract

Background: Peritonitis is a common complication in which the peritoneum becomes inflamed. Peroxisome proliferator-activated receptor (PPAR)γ agonists and extracellular signal-regulated kinases 1/2 (ERK1/2) inactivation have been found to restore damage caused by lipopolysaccharide-induced (LPS) inflammation. This study aimed to investigate the association between PPARγ and ERK1/2 in LPS-induced inflammation in peritonitis. Methods: Human peritoneal mesothelial cells were maintained in Dulbecco's Modified Eagle Medium and treated with LPS under a series of different concentrations and treatment times. Cellular interleukins-1βeta (IL-1β), cellular interleukins-6 (IL-6), cellular interleukins-12 (IL-12) were measured by enzyme-linked immunosorbent assay (ELISA) assay. Expression or activation of cyclin-dependent kinase (CDK)5, ERK1/2, and PPARγ was detected using quantitative real-time PCR and/or western blot. Results: LPS induced dose-and time-dependent increments in the cellular IL-1β, IL-6, and IL-12 contents, cyclin-dependent kinase 5 (CDK5) expression, and PPARγ Ser273 phosphorylation. Treatment