PARK7 Is Required to Protect Epithelia Against Damage in Oral Lichen Planus

To investigate the roles of Parkinson disease protein 7 (PARK7) in the context of oral lichen planus (OLP).

Real-time PCR and western blot were performed to detect the expression of PARK7. Chromatin Immunoprecipitation (ChIP) and luciferase reporter assays were conducted to confirm the binding of p65 and NF-κB element in the promoter of the human PARK7 gene. The Caspase 3 and NF-κB detection kits were used for Caspase 3 and NF-κB activities measurement. Co-Immunoprecipitation (Co-IP) was applied to test the protein-protein interactions in HOKs.

The levels of PARK7 were up-regulated in the diseased oral keratinocytes derived from OLP patients compared to those from healthy donors. Mechanistically, the activated NF-κB pathway could increase PARK7 gene transcription in human oral keratinocytes (HOKs). Moreover, PARK7 deletion facilitated cell apoptosis and NF-κB activation in HOKs under OLP conditions. Overexpression of PARK7 could suppress cell apoptosis and NF-κB activation in the OLP cell model. At the molecular level, PARK7 could interact with BAX and p65 to inhibit cell apoptosis and NF-κB activation in HOKs, respectively.

Our data indicate that PARK7 is required to protect epithelia against damage in oral lichen planus.