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Leptin attenuates hypoxia‐induced apoptosis in human periodontal ligament cells via the reactive oxygen species–hypoxia‐inducible factor‐1α pathway
Author(s) -
Gao Jing,
Zhu Junfei,
Zhao Yuwei,
Gan Xueqi,
Yu Haiyang
Publication year - 2021
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep089324
Subject(s) - apoptosis , leptin , hypoxia (environmental) , periodontal fiber , reactive oxygen species , microbiology and biotechnology , chemistry , hypoxia inducible factors , endocrinology , biology , medicine , oxygen , biochemistry , dentistry , organic chemistry , gene , obesity
New FindingsWhat is the central question of this study? Does leptin have an effect on hypoxia‐induced apoptosis in human periodontal ligament cells (hPDLCs), and what is the potential underlying mechanism?What is the main finding and its importance? Hypoxia induces cell apoptosis and leptin expression in hPDLCs through the induction of hypoxia‐inducible factor‐1α and accumulation of reactive oxygen species (ROS). Leptin shows feedback inhibition on hypoxia‐induced ROS‐mediated apoptosis in hPDLCs, suggesting a new application of leptin for hypoxic damage in periodontal diseases.Abstract Hypoxia‐induced apoptosis of human periodontal ligament cells (hPDLCs) is an important contributor to the progression of various periodontal diseases. Although leptin has been shown to protect connective tissue cells against hypoxia‐induced injury, whether it might do so by attenuating hypoxia‐induced apoptosis in hPDLCs remains unclear. Here, using CoCl 2 treatment, we simulated hypoxic conditions in hPDLCs and explored whether apoptosis and reactive oxygen species (ROS) levels were related to hypoxia. After small interfering RNA (siRNA) inhibition of leptin and hypoxia‐inducible factor‐1α (HIF‐1α), the levels of apoptosis, ROS and leptin expression were measured. We showed that in CoCl 2 ‐treated hPDLCs, significantly higher cell apoptosis rates and ROS accumulation were observed. Cobalt chloride also increased leptin and HIF‐1α expression in hPDLCs. Further investigation of the pathway demonstrated that inhibition of ROS attenuated hypoxia‐induced cell apoptosis and leptin expression, whereas siRNA inhibition of leptin aggravated hypoxia‐induced cell apoptosis and ROS accumulation. Hypoxia induces cell apoptosis and leptin expression in hPDLCs through the induction of ROS and HIF‐1α pathways, and leptin shows feedback inhibition on ROS‐mediated apoptosis in hPDLCs. These findings suggest a new application of leptin for hypoxic damage in periodontal diseases.