Endoplasmic reticulum stress mediates osteocyte death under oxygen-glucose deprivation in vitro
Autor: | Junhui Ding, Yizhong Wang, Chen Qiu, Bing Han, Wenbo Wang |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Programmed cell death Histology Cell Survival Blotting Western Apoptosis medicine.disease_cause Osteocytes 03 medical and health sciences Mice 0302 clinical medicine medicine Animals Cell damage Cell Death Chemistry Endoplasmic reticulum Cell Biology General Medicine medicine.disease Endoplasmic Reticulum Stress Cell biology Oxygen Oxidative Stress 030104 developmental biology medicine.anatomical_structure Glucose 030220 oncology & carcinogenesis Osteocyte Unfolded protein response Reactive Oxygen Species Intracellular Oxidative stress |
Zdroj: | Acta histochemica. 122(6) |
ISSN: | 1618-0372 |
Popis: | As a vascularized organ, bone is known to be susceptible to ischemia. Ischemic osteonecrosis or skeletal unloading lead to ischemia in bone microenvironment that causes osteocytes to suffer hypoxia and nutrition deprivation. Objective To explore the effects of Oxygen-glucose deprivation (OGD) on osteocytes and the potential mechanism. Methods OGD model was established in cultured MLO-Y4 cell. Cell damage, intracellular oxidative stress and cell apoptosis were detected at different OGD times (0, 2, 4, 8, 12, 24 h), and the changes in endoplasmic reticulum (ER) stress-related indicators were observed. Furthermore, cells were treated with 4-phenylbutyrate sodium (4-PBA) to inhibit ER stress, and cell damage and oxidative stress level were detected. Results The cell viability under OGD exhibited a significantly reduced in a time-dependent manner, and the level of intracellular reactive oxygen species (ROS) were increased, cell apoptosis and ER stress was induced. Inhibition of ER stress can reduce cell death and intracellular ROS levels. Conclusion Our study demonstrated that ER stress regulates OGD-induced apoptotic cell death in MLO-Y4 cells via intracellular ROS. |
Databáze: | OpenAIRE |
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