GOLPH3 Mediated Golgi Stress Response in Modulating N2A Cell Death upon Oxygen-Glucose Deprivation and Reoxygenation Injury

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• 作者：Ting Li ; Hong You ; Xiaoye Mo ; Wenfang He ; Xiangqi Tang…
• 关键词：GOLPH3 ; Ischemia/reperfusion ; Oxygen ; glucose deprivation and reoxygenation (OGD/R) ; Golgi stress response ; Reactive oxygen species (ROS) ; Autophagy ; ER stress ; Apoptosis ; Mitochondria ; Oxidative stress
• 刊名：Molecular Neurobiology
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：53
• 期：2
• 页码：1377-1385
• 全文大小：875 KB
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• 作者单位：Ting Li (1)
  Hong You (1)
  Xiaoye Mo (1)
  Wenfang He (1)
  Xiangqi Tang (1)
  Zheng Jiang (1)
  Shiyu Chen (1)
  Yang Chen (1)
  Jie Zhang (1)
  Zhiping Hu (1)
  
  1. The Second Xiangya Hospital Central South University, Changsha, Hunan, China
  
• 刊物主题：Neurosciences; Neurobiology; Cell Biology; Neurology;
• 出版者：Springer US
• ISSN：1559-1182

文摘

Increasing evidence implicating that the organelle-dependent initiation of cell death merits further research. The evidence also implicates Golgi as a sensor and common downstream-effector of stress signals in cell death pathways, and it undergoes disassembly and fragmentation during apoptosis in several neurological disorders. It has also been reported that during apoptotic cell death, there is a cross talk between ER, mitochondria, and Golgi. Thus, we hypothesized that Golgi might trigger death signals during oxidative stress through its own machinery. The current study found that GOLPH3, an outer membrane protein of the Golgi complex, was significantly upregulated in N2A cells upon oxygen-glucose deprivation and reoxygenation (OGD/R), positioning from the compact perinuclear ribbon to dispersed vesicle-like structures throughout the cytoplasm. Additionally, elevated GOLPH3 promoted a stress-induced conversion of the LC3 subunit I to II and reactive oxygen species (ROS) production in long-term OGD/R groups. The collective data indicated that GOLPH3 not only acted as a sensor of Golgi stress for its prompt upregulation during oxidative stress but also as an initiator that triggered and propagated specific Golgi stress signals to downstream effectors. This affected ROS production and stress-related autophagy and finally controlled the entry into apoptosis. The data also supported the hypothesis that the Golgi apparatus could be an ideal target for stroke, neurodegenerative diseases, or cancer therapy through its own functional proteins. Keywords GOLPH3 Ischemia/reperfusion Oxygen-glucose deprivation and reoxygenation (OGD/R) Golgi stress response Reactive oxygen species (ROS) Autophagy ER stress Apoptosis Mitochondria Oxidative stress