RhoGDI2 Expression in Astrocytes After an Excitotoxic Lesion in the Mouse Hippocampus

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• 作者：Min-Hee Yi (1)
  Kisang Kwon (2)
  Enji Zhang (1)
  Je Hoon Seo (3)
  Sang Soo Kang (4)
  Chang-Gue Son (5)
  Joon Won Kang (6)
  Dong Woon Kim (1)
  
  1. Department of Anatomy ; Brain Research Institute ; Chungnam National University School of Medicine ; Daejeon ; 301-747 ; South Korea
  2. Department of Biomedical Laboratory Science ; College of Health & Welfare ; Kyungwoon University ; Gumi ; 730-739 ; Korea
  3. Department of Anatomy ; School of Medicine ; Chungbuk National University ; Cheongju ; 361-763 ; South Korea
  4. Department of Anatomy and Neurobiology ; Institute of Health Sciences ; Medical Research Center for Neural Dysfunction ; School of Medicine ; Gyeongsang National University ; Jinju ; 660-702 ; South Korea
  5. Liver and Immunology Research Center ; Korean Medical College of Daejeon University ; Daejeon ; 300-716 ; South Korea
  6. Department of Pediatrics ; Chungnam National University Hospital ; Daejeon ; 301-721 ; South Korea
  
• 关键词：RhoGDI2 ; Astrocyte migration ; PKB ; Kainic acid ; Excitotoxicity
• 刊名：Cellular and Molecular Neurobiology
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：35
• 期：2
• 页码：167-174
• 全文大小：1,296 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Animal Anatomy, Morphology and Histology
  
• 出版者：Springer Netherlands
• ISSN：1573-6830

文摘

The Rho GDP-dissociation inhibitor (RhoGDI) originally downregulates Rho family GTPases by preventing nucleotide exchange and membrane association. Although RhoGDI2 functions as a metastasis regulator, little is known in glial cells under neuropathological conditions. We monitored RhoGDI2 expression in the mouse brain after administering a kainic acid(KA)-induced excitotoxic lesion. In control, RhoGDI2 immunoreactivity (IR) was evident in the neuronal layer of the hippocampus. However, RhoGDI2 IR was increased in astrocytes markedly throughout the hippocampus at day 3 post-treatment with KA. To further investigate the molecular mechanism of RhoGDI2-induced cellular migration, primary astrocytes were transfected with the flag-tagged RhoGDI2 cDNA. Cell migration assay revealed that RhoGDI2 cDNA transfection inhibits astrocyte migration. Overexpression of RhoGDI2 leads to inhibit protein kinase B (PKB) activation and cdc42 and cAMP-responsive element-binding protein (CREB) phosphorylation. In conclusion, our results suggested for the first time that RhoGDI2 is required for PKB and CREB activation and cdc42 expression in astrocyte migration after KA-mediated excitotoxic lesion in mouse brain.