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EphrinB2-EphB2 signaling for dendrite protection after neuronal ischemia in vivo and oxygen-glucose deprivation in vitro

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机构： [1]Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA [2]Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China [3]Cerebrovascular Research Institute, Xuanwu Hospital, Capital Medical University, Beijing, China [4]Clinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA, USA

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关键词： dendrites EphB2 ephrinB2 ischemia oxygen-glucose deprivation

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In order to rescue neuronal function, neuroprotection should be required not only for the neuron soma but also the dendrites. Here, we propose the hypothesis that ephrin-B2-EphB2 signaling may be involved in dendritic degeneration after ischemic injury. A mouse model of focal cerebral ischemia with middle cerebral artery occlusion (MCAO) method was used for EphB2 signaling test in vivo. Primary cortical neuron culture and oxygen-glucose deprivation were used to assess EphB2 signaling in vitro. siRNA and soluble ephrin-B2 ectodomain were used to block ephrin-B2-Ephb2 signaling. In the mouse model of focal cerebral ischemia and in neurons subjected to oxygen-glucose deprivation, clustering of ephrin-B2 with its receptor EphB2 was detected. Phosphorylation of EphB2 suggested activation of this signaling pathway. RNA silencing of EphB2 prevented neuronal death and preserved dendritic length. To assess therapeutic potential, we compared the soluble EphB2 ectodomain with the NMDA antagonist MK801 in neurons after oxygen-glucose deprivation. Both agents equally reduced lactate dehydrogenase release as a general marker of neurotoxicity. However, only soluble EphB2 ectodomain protected the dendrites. These findings provide a proof of concept that ephrin-B2-EphB2 signaling may represent a novel therapeutic target to protect both the neuron soma as well as dendrites against ischemic injury. © The Author(s) 2020.

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出版当年[2020]版：

大类 | 2 区医学

小类 | 2 区内分泌学与代谢 2 区血液学 2 区神经科学

最新[2023]版：

大类 | 2 区

医学

小类 | 2 区内分泌学与代谢 2 区血液学 2 区神经科学

JCR分区：

出版当年[2019]版：

Q1 ENDOCRINOLOGY & METABOLISM Q1 NEUROSCIENCES Q1 HEMATOLOGY

最新[2023]版：

Q1 ENDOCRINOLOGY & METABOLISM Q1 HEMATOLOGY Q1 NEUROSCIENCES

影响因子： 4.9 最新[2023版] 6.1 最新五年平均 5.681 出版当年[2019版] 5.787 出版当年五年平均 6.04 出版前一年[2018版] 6.2 出版后一年[2020版]

第一作者：

第一作者机构： [1]Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA [*1]Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Room 2401, Charlestown, MA 02129, USA.

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通讯作者：

通讯机构： [*1]Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Room 2401, Charlestown, MA 02129, USA.

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EphrinB2-EphB2 signaling for dendrite protection after neuronal ischemia in vivo and oxygen-glucose deprivation in vitro

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