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

被引:24
作者
Feng, Hao [1 ]
Li, Ziyu [1 ]
Du, Juan [1 ]
Sun, Jing [1 ]
Feng, Wei [2 ]
Li, Dongfang [1 ]
Lui, Shanshan [1 ]
Wang, Wei [1 ]
Liu, Hongrui [1 ]
Amizuka, Norio [3 ]
Li, Minqi [1 ]
机构
[1] Shandong Univ, Dept Bone Metab, Sch Stomatol, Shandong Prov Key Lab Oral Tissue Regenerat, Jinan, Shandong, Peoples R China
[2] Jinan Stomatol Hosp, Dept Endodont, Jinan, Shandong, Peoples R China
[3] Hokkaido Univ, Grad Sch Dent Med, Dept Dev Biol Hard Tissue, Sapporo, Hokkaido, Japan
关键词
ENDOTHELIAL APOPTOSIS; OXIDATIVE STRESS; BONE-RESORPTION; ROLES; DIFFERENTIATION; CANCER;
D O I
10.1038/s41420-018-0050-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Lipopolysaccharide (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 (Prx1(KO)) and Prx1 overexpression (Prx1(OE)) cells compared with wild type. After LPS stimulation, intracellular ROS in Prx1(KO) cells showed the highest level and Prx1(OE) cells showed the least. Treatment with LPS significantly elevated the expression of Bax, Cyto-c, and caspase 3 in Prx1(KO) cells compared with wild type, although this could be completely abolished by NAC. In Prx1(OE) cells, 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 H2O2 messenger, triggering the expression of ASK1 and its downstream cascades.
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页数:11
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