Long-term blue light exposure induces RGC-5 cell death in vitro: involvement of mitochondria-dependent apoptosis, oxidative stress, and MAPK signaling pathways

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• 作者：Chen Huang (1) (2)
  Pei Zhang (1)
  Wei Wang (1)
  Yongsheng Xu (1) (3)
  Minshu Wang (1)
  Xiaoyong Chen (1)
  Xuran Dong (1)
  
• 关键词：Blue light ; Retinal ganglion cell ; RGC ; 5 ; Oxidative stress ; Apoptosis ; MAPK
• 刊名：Apoptosis
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：19
• 期：6
• 页码：922-932
• 全文大小：2,425 KB
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• 作者单位：Chen Huang (1) (2)
  Pei Zhang (1)
  Wei Wang (1)
  Yongsheng Xu (1) (3)
  Minshu Wang (1)
  Xiaoyong Chen (1)
  Xuran Dong (1)
  
  1. Department of Ophthalmology, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China
  2. Medical Research Center, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China
  3. Clinical Stem Cell Center, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China
  
• ISSN：1573-675X

文摘

The mechanism of blue light-induced retinal ganglion cell (RGC) injury is poorly understood. In this study, we established a patented light-emitting diode-based system to study the effects of long-term blue light exposure under culture conditions on RGC-5 cells. Long-term blue light exposure significantly reduced cell viability in a time-dependent manner and induced apoptosis and necrosis in RGC-5 cells. Long-term blue light exposure marked an increase in the expression of Bax and active Caspase-3 (p17), which was accompanied by Bcl-2 down-regulation, and displayed features of the mitochondria-dependent apoptosis pathway. Blue light exposure also increased the generation of reactive oxygen species (ROS), and was a strong inducer of ROS-sensitive protein nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Moreover, blue light exposure constitutively activated p38 mitogen-activated protein kinases and c-Jun NH2-terminal kinase (JNK), as well as induced the phosphorylation of extracellular signal-regulated kinase in the early phase, in blue light-exposed RGC-5 cells. The protein expression of c-jun and c-fos was further enhanced after RGC-5 cells were exposed to blue light. Taken together, these findings indicated that blue light induced RGC-5 cell line death in dependence upon exposure duration. The potential mechanisms for this phenomenon might be via activated mitochondria-dependent apoptosis, increased ROS production and protein expressions of Nrf2 and HO-1, and activated JNK/p38 MAPK signaling pathways.