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Blocking the EGFR/p38/NF-κB signaling pathway alleviates disruption of BSCB and subsequent inflammation after spinal cord injury.

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收录情况： ◇ SCIE

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机构： [1]Department of Neurology, Shenzhen People’s Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, 518020, PR China [2]Center of Clinical Research, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, 214023, PR China [3]Department of Neurology, Shanghai Fourth People’s Hospital, School of Medicine, Tongji University, Shanghai, 200434, PR China [4]Department of Neurology, Yancheng First People’s Hospital, Yancheng, 224001, PR China [5]University of Traditional Chinese Medicine, Kunming, 650500, PR China [6]Otolaryngological Department, Yunnan Province Traditional Chinese Medicine, Hospital of Yunnan University of Traditional Chinese Medicine, Kunming, 650500, PR China

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关键词： Spinal cord injury Blood spinal cord barrier Epidermal growth factor receptor Secondary inflammatory injury

摘要：

Epidermal growth factor receptor (EGFR) activation is involved in blood spinal cord barrier (BSCB) disruption and secondary injury after spinal cord injury (SCI). However, the underlying mechanisms of EGFR activation mediating BSCB disruption and secondary injury after SCI remain unclear. An in vitro model of oxygen and glucose deprivation/reoxygenation (OGD/R) induced BSCB damage and in vivo rat SCI model were employed to define the role of EGFR/p38/NF-κB signal pathway activation and its induced inflammatory injury in main cellular components of BSCB. Genetic regulation (lentivirus delivered shRNA and overexpression system) or chemical intervention (agonist or inhibitor) were applied to activate or inactivate EGFR and p38 in astrocytes and microvascular endothelial cells (MEC) under which conditions, the expression of pro-inflammatory factors (TNF-α, iNOS, COX-2, and IL-1β), tight junction (TJ) protein (ZO-1 and occludin), nuclear translocation of NF-κB and permeability of BSCB were analyzed. The pEGFR was increased in astrocytes and MEC which induced the activation of EGFR and p38 and NF-κB nuclear translocation. The activation of EGFR and p38 increased the TNF-α, iNOS, COX-2, and IL-1β responsible for the inflammatory injury and reduced the ZO-1 and occludin which caused BSCB disruption. While EGFR or p38 inactivation inhibited NF-κB nuclear translocation, and markedly attenuated the production of pro-inflammatory factors and the loss of TJ protein. This study suggests that the EGFR activation in main cellular components of BSCB after SCI mediates BSCB disruption and secondary inflammatory injury via the EGFR/p38/NF-κB pathway.Copyright © 2021 Elsevier Ltd. All rights reserved.

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出版当年[2021]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

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[2020]版：

Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 NEUROSCIENCES

最新[2023]版：

Q1 NEUROSCIENCES Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 4.4 最新[2023版] 3.8 最新五年平均 3.921 出版当年[2020版] 4.539 出版当年五年平均 3.881 出版前一年[2019版] 4.297 出版后一年[2021版]

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第一作者机构： [1]Department of Neurology, Shenzhen People’s Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, 518020, PR China

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Blocking the EGFR/p38/NF-κB signaling pathway alleviates disruption of BSCB and subsequent inflammation after spinal cord injury.

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