Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway

• DOI: 10.1038/s41420-018-0050-9
• Publication Date: 2018-04-23T07:26:41Z
• Authors: Hao Feng; Ziyu Li; Juan Du; Jing Sun; Wei Feng; Dongfang Li; Shanshan Liu; Wei Wang; Hongrui Liu; Norio Amizuka; Minqi Li
• Keywords: 0303 health sciences; 03 medical and health sciences; Article

AbstractLipopolysaccharide (LPS)-induced osteoblast apoptosis is a prominent factor to the defect in periodontal tissue repair in periodontal disease. LPS challenge contributes to the production of reactive oxygen species (ROS) in periodontitis, and peroxiredoxin 1 (Prx1) is an antioxidant protein that protect cells against oxidative damage from ROS. Without LPS stimulation, apoptotic rates were higher in both Prx1 knockout (Prx1KO) and Prx1 overexpression (Prx1OE) cells compared with wild type. After LPS stimulation, intracellular ROS in Prx1KOcells showed the highest level and Prx1OEcells showed the least. Treatment with LPS significantly elevated the expression of Bax, Cyto-c, and caspase 3 in Prx1KOcells compared with wild type, although this could be completely abolished by NAC. In Prx1OEcells, the expression and activation of ASK1 were significantly increased, and this was slightly reduced by LPS stimulation. NQDI-1 completely abolished the increased phosphorylation of JNK and p38 and the expression of caspase 3 in LPS-stimulated cells. These results indicate that Prx1 eliminates intracellular ROS and exhibits a cytoprotective role in LPS-induced apoptosis. However, under physiological conditions, Prx1 overexpression acts as a H2O2messenger, triggering the expression of ASK1 and its downstream cascades.