Up-Regulation of KPNB1 Involves in Neuronal Apoptosis Following Intracerebral Hemorrhage in Adult Rats

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• 作者：Aihua Dai ; Xiaorong Liu ; Yu Zhang ; Lijian Han ; Liang Zhu…
• 关键词：Intracerebral hemorrhage (ICH) ; Kpnb1 ; Apoptosis ; Adult rats
• 刊名：Neurochemical Research
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：40
• 期：11
• 页码：2177-2187
• 全文大小：3,973 KB
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• 作者单位：Aihua Dai (1)
  Xiaorong Liu (1)
  Yu Zhang (1)
  Lijian Han (1)
  Liang Zhu (1)
  Haidan Ni (1)
  Rongrong Chen (1)
  Maohong Cao (1)
  
  1. Department of Neurology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Kpnb1, also known as Importin β1, is a member of the Karyopherin protein family which plays a important role in nuclear import and export pathways. Its expression has been shown to be responsive to stress, such as heat shock, ethanol and oxidative stress. Previous studies demonstrated that Kpnb1 had anti-apoptotic in cervical cancer. These together prompted us to explore whether Kpnb1 has some association with neuron apoptosis in the pathophysiology of intracerebral hemorrhage (ICH). In our study, an ICH model was established by injecting into the right basal ganglia of adult rats with their autologous whole blood and assessed by behavioral tests. We found Kpnb1 were significantly up-regulated adjacent to the hematoma following ICH by Western blot and immunohistochemistry. Double immunofluorenscence manifested Kpnb1 was strikingly increased in neurons, not astrocytes or microglia. Furthermore, we also found that kpnb1 had co-localizations with active-caspase-3 which is a neuronal apoptosis marker suggesting its role in neuronal apoptosis. What’s more, our in vitro study, using Kpnb1 RNA interference in PC12 cells, further indicated that Kpnb1 might exert its pro-apoptotic function on neuronal apoptosis. Therefore, Kpnb1 may play a role in the neuronal apoptosis following ICH.