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Autophagy inhibition preserves tight junction of human cerebral microvascular endothelium under oxygen glucose deprivation.

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机构： [1]Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China [2]Departmentof Anesthesiology, Shenzhen University General Hospital, Shenzhen, China [3]Department of Anesthesiology andCritical Care, Perelman School of Medicine at the University of Pennsylvania, Philadelphia PA, USA

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To investigate the role of autophagy in the tight junction of human brain endothelial cells during hypoxia and ischemia. Endothelial cells play an important role in the initiation, progression and recovery from ischemic stroke. The role of autophagy on human brain endothelial cells (HBECs) subjected to oxygen-glucose deprivation (OGD) is not fully elucidated. The objective of this study was to investigate the effect of autophagy on HBECs during OGD. HBECs were cultured in a 96-well plate and underwent 4 hours of OGD. For drug treatment, 3-Methyladenine (3- MA) (5mmol/L), an inhibitor of autophagy, was added at the start of OGD. Cell viability and cytotoxicity were tested by cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) assays. Morphological changes in cells were examined by immunofluorescence microscopy. The protein expression of light chain 3 (LC3) was measured. Autophagosomes and endothelial cell tight junctions were observed using transmission electron microscopy. The results showed that OGD induced serious damage to HBECs. Cell viability was decreased significantly and LDH release increased significantly (p<0.05) following OGD. 3-MA protected HBECs from damage. Immunostaining further confirmed these results. Since 3-MA is an inhibitor of autophagy, we chose to examine alterations in the amount of LC3, a marker of autophagy. The ratios of LC3-Ⅱ to LC3-Ⅰwere significantly lower in the 3-MA treated OGD group than in the non-3-MA treated OGD group (p<0.05). Electron microscopy showed that 3-MA inhibited the formation of autophagolysosomes and revealed that the tight junction ultrastructure of HBECs, which was destroyed by OGD, was significantly protected by treatment with 3-MA. Autophagy is a key response to oxygen-glucose deprivation stress and its detrimental effects are closely related with destruction of tight junctions of human brain endothelial cells. Strategies to inhibit autophagy could help to preserve tight junctions. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

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出版当年[2020]版：

大类 | 4 区医学

小类 | 4 区临床神经病学 4 区神经科学

最新[2025]版：

大类 | 4 区医学

小类 | 4 区临床神经病学 4 区神经科学

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出版当年[2019]版：

Q4 CLINICAL NEUROLOGY Q4 NEUROSCIENCES

最新[2024]版：

Q3 CLINICAL NEUROLOGY Q4 NEUROSCIENCES

影响因子： 1.7 最新[2024版] 2 最新五年平均 1.649 出版当年[2019版] 1.876 出版当年五年平均 1.811 出版前一年[2018版] 1.99 出版后一年[2020版]

第一作者：

第一作者机构： [1]Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China [3]Department of Anesthesiology andCritical Care, Perelman School of Medicine at the University of Pennsylvania, Philadelphia PA, USA

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通讯机构： [3]Department of Anesthesiology andCritical Care, Perelman School of Medicine at the University of Pennsylvania, Philadelphia PA, USA [*1]Department of Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania, PhiladelphiaPA, USA

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