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.