JNK and AKT/GSK3β signaling pathways converge to regulate periodontal ligament cell survival involving XIAP

•PDLCs apoptosis model was induced by the exposure of cells to 250 μM H2O2 for 72 h.•The levels of XIAP, Akt, pAkt, JNK2, and GSK3β were reduced by the incubation with H2O2.•Reductions induced by H2O2 were partially recovered in PDLCs overexpressing XIAP.•These reductions (except for pAKT) were mimicked by RNA interference of XIAP.

Periodontal ligament cells (PDLCs) were incubated with H2O2 and the levels of XIAP protein, protein kinase B (AKT), phosphorylated forms of AKT (pAKT), c-Jun N-terminal kinase (JNK), and glycogen synthase kinase-3β (GSK3β) were determined by western immunoblotting or immunocytochemistry. After overexpression and knockdown of XIAP, the AKT, pAKT, JNK and GSK3β levels were determined in PDLCs exposed to H2O2.We demonstrated that 72 h of 250 μM H2O2 exposure resulted in an increase in apoptosis. Meanwhile, XIAP levels were decreased with 72 h of 250 μM H2O2 exposure, while there were also a decrease of JNK2, AKT, pAKT, and GSK3β levels. Such reductions induced by 72 h of 250 μM H2O2 treatment were partially recovered in PDLCs overexpressing XIAP. Interestingly, these reductions (except for pAKT) were mimicked by RNA interference of XIAP. These results suggest that, after 72 h of 250 μM H2O2 exposure, Akt, JNK, and GSK3β intracellular kinase signaling pathways converge to regulate PDLC survival involving XIAP.