Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (1): 64-69.doi: 10.3969/j.issn.1673-5374.2013.01.008

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Expression of netrin-1 and its receptors, deleted in colorectal cancer and uncoordinated locomotion-5 homolog B, in rat brain following focal cerebral ischemia reperfusion injury

Xiaodan Wang1, 2, Jinming Xu2, Jieqin Gong2, Hui Shen2, Xiaoping Wang1   

  1. 1 Department of Neurology, Shanghai First People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
    2 Department of Neurology, Suzhou Kowloon Hospital, Shanghai Jiao Tong University School of Medicine, Suzhou 215028, Jiangsu Province, China
  • Received:2012-08-20 Revised:2012-11-14 Online:2013-01-05 Published:2013-01-05
  • Contact: Xiaoping Wang, M.D., Chief physician, Professor, Doctoral supervisor, Department of Neurology, Shanghai First People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China, window_xp@ 126.com.
  • About author:Xiaodan Wang, Attending physician.
  • Supported by:

    This study was supported by the Science and Technology Program of Suzhou Industrial Park in China.

Abstract:

Netrin-1 is currently one of the most highly studied axon guidance factors. Netrin-1 is widely expressed in the embryonic central nervous system, and together with the deleted in colorectal cancer and uncoordinated locomotion-5 homolog B receptors, netrin-1 plays a guiding role in the construction of neural conduction pathways and the directional migration of neuronal cells. In this study, we established a rat middle cerebral artery ischemia reperfusion model using the intraluminal thread technique. Immunofluorescence microscopy showed that the expression of netrin-1 and deleted in colorectal cancer in the ischemic penumbra was upregulated at 1 day after reperfusion, reached a peak at 14 days, and decreased at 21 days. There was no obvious change in the expression of uncoordinated locomotion-5 homolog B during this time period. Double immunofluorescence labeling revealed that netrin-1 was expressed in neuronal cells and around small vessels, but not in astrocytes and microglia, while deleted in colorectal cancer was localized in the cell membranes and protrusions of neurons and astrocytes. Our experimental findings indicate that netrin-1 may be involved in post-ischemic repair and neuronal protection via deleted in colorectal cancer receptors.

Key words: neural regeneration, brain injury, cerebral ischemia and reperfusion, netrin-1, uncoordinated locomotion-5 homolog B, deleted in colorectal cancer, neuron, brain injury, grant-supported paper, photographs-containing paper, neuroregeneration