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Ischemic neurons activate astrocytes to disrupt endothelial barrier via increasing VEGF expression

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收录情况： ◇ SCIE

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机构： [1]Department of Geriatrics, The Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, China [2]Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico,Albuquerque, New Mexico, USA [3]Department of Toxicology, School of Preventive Medicine, The Fourth Military Medical University,Xi’an, China [4]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University,Beijing, China [5]Central Laboratory of Shenzhen Second People’s Hospital, the First Affiliated Hospital of Shenzhen University, Shenzhen, China

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关键词： astrocyte blood-brain barrier neuron oxygen-glucose deprivation VEGF

摘要：

Blood-brain barrier (BBB) disruption occurring within the first few hours of ischemic stroke onset is closely associated with hemorrhagic transformation following thrombolytic therapy. However, the mechanism of this acute BBB disruption remains unclear. In the neurovascular unit, neurons do not have direct contact with the endothelial barrier; however, they are highly sensitive and vulnerable to ischemic injury, and may act as the initiator for disrupting BBB when cerebral ischemia occurs. Herein, we employed oxygen-glucose deprivation (OGD) and an in vitro BBB system consisting of brain microvascular cells and astrocytes to test this hypothesis. Neurons (CATH.a cells) were exposed to OGD for 3-h before co-culturing with endothelial monolayer (bEnd 3 cells), or endothelial cells plus astrocytes (C8-D1A cells). Incubation of OGD-treated neurons with endothelial monolayer alone did not increase endothelial permeability. However, when astrocytes were present, the endothelial permeability was significantly increased, which was accompanied by loss of occludin and claudin-5 proteins as well as increased vascular endothelial growth factor (VEGF) secretion into the conditioned medium. Importantly, all these changes were abolished when VEGF was knocked down in astrocytes by siRNA. Our findings suggest that ischemic neurons activate astrocytes to increase VEGF production, which in turn induces endothelial barrier disruption.

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出版当年[2013]版：

大类 | 2 区

医学

小类 | 3 区生化与分子生物学 3 区神经科学

最新[2023]版：

大类 | 3 区医学

小类 | 3 区生化与分子生物学 3 区神经科学

JCR分区：

出版当年[2012]版：

Q2 NEUROSCIENCES Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

最新[2023]版：

Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 NEUROSCIENCES

影响因子： 4.2 最新[2023版] 4.9 最新五年平均 3.973 出版当年[2012版] 4.25 出版当年五年平均 4.061 出版前一年[2011版] 4.244 出版后一年[2013版]

第一作者：

第一作者机构： [1]Department of Geriatrics, The Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, China

通讯作者：

通讯机构： [*1]College of Pharmacy, University of New Mexico, Albuquerque, NM 87131- 0001, USA. [*2]the Central Laboratory of Shenzhen Second People’s Hospital (the First Affiliated Hospital of Shenzhen University), Shenzhen, 518035, China.

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Ischemic neurons activate astrocytes to disrupt endothelial barrier via increasing VEGF expression

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