Periostin inhibits hypoxia-induced oxidative stress and apoptosis in human periodontal ligament fibroblasts p38 MAPK signaling pathway.
- Author:
Huili LIU
1
;
Yidan WANG
1
;
Yangli YUE
2
;
Peng ZHANG
2
;
Yali SUN
1
;
Qiaohua CHEN
1
Author Information
1. Department of Stomatology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.
2. School of Stomatology, Zhengzhou University, Zhengzhou 450007, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Adhesion Molecules;
administration & dosage;
Cell Hypoxia;
Fibroblasts;
drug effects;
Humans;
Oxidative Stress;
drug effects;
Periodontal Ligament;
cytology;
Signal Transduction;
drug effects;
p38 Mitogen-Activated Protein Kinases
- From:
Journal of Zhejiang University. Medical sciences
2020;40(7):942-948
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of periostin on hypoxia-induced oxidative stress and apoptosis in human periodontal ligament fibroblasts and the molecular mechanism involved.
METHODS: cultured human periodontal ligament fibroblasts were placed in an anaerobic gas-producing bag for hypoxia treatment for 48 h followed by treatment with periostin at low (25 ng/mL), moderate (50 ng/mL) or high (100 ng/mL) doses. MTT assay was used to measure the cell viability, and the cell apoptosis rate was determined using flow cytometry. The contents of IL-1β, IL-6 and TNF-α in the cells were determined with ELISA, and ROS levels were measured using a fluorescent plate reader. The intracellular SOD activity was detected using ELISA. The expressions of HIF-1α, P21, cyclin D1, Bax, cleaved caspase-3, Bcl-2, P38MAPK and p-p38 MAPK proteins in the cells were detected with Western blotting.
RESULTS:Hypoxia treatment significantly reduced the cell viability ( < 0.05), increased P21, Bax, and cleaved caspase-3 protein levels ( < 0.05), promoted cell apoptosis ( < 0.05), and decreased cyclin D1 and Bcl-2 protein levels ( < 0.05) in the cells. Compared with the hypoxic group, the cells treated with periostin at different concentrations showed significantly increased cell viability ( < 0.05) with significantly lowered apoptotic rates ( < 0.05) and decreased expression levels of Bax and cleaved caspase-3 ( < 0.05) but significantly increased expression levels of cyclin D1 and Bcl-2 ( < 0.05). Hypoxic exposure of the cells resulted in significantly increased expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and increased levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) but decreased SOD activity ( < 0.05). Periostin treatment at different concentrations significantly lowered the expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and the levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) and significantly increased SOD activity in the hypoxic cells ( < 0.05).
CONCLUSIONS:Periostin promotes the proliferation, inhibits apoptosis, enhances cellular antioxidant capacity, and reduces inflammatory damage in human periodontal ligament fibroblasts exposed to hypoxia possibly by inhibiting the activation of the p38 MAPK signaling pathway.
