Acetylation of HMGB1 by JNK1 Signaling Promotes LPS-Induced Peritoneal Mesothelial Cells Apoptosis.

摘要: Increased high mobility group box 1 (HMGB1) in dialysis effluence is associated with the presence of peritoneal dialysis-related peritonitis patients and dysfunction acute mice model, but it remains unclear whether HMGB1 involved mesothelial cell injury functions via molecular posttranslational modifications by acetylation this process. Here we first showed correlation between level occurrence Gram-negative peritonitis. The increased acetylated was similarly observed under lipopolysaccharides (LPS) treatment both human line (HMrSV5) visceral peritoneum tissue. Overexpression wild-type, not hypoacetylation mutant HMGB1, enhanced LPS-induced apoptosis HMrSV5 cells, which accompanied elevated protein levels BAX cleaved-caspase 3 compared to control. Pretreatment JNK inhibitor attenuated acetylation. Consistently, primary cells from Jnk1-/- a lower contents fewer apoptosis, decreased expression cleaved-caspase3 after LPS exposure, as those wild-type mice. In conclusion, our data demonstrated promotes JNK1-mediated upregulation