Fibronectin and neuroprotective effect of granulocyte colony-stimulating factor in focal cerebral ischemia

• Published in: Brain research 2006-07, Vol.1098 (1), p.161-169
• Main Authors: Yanqing, Zhao, Yu-Min, Luo, Jian, Qiao, Bao-Guo, Xiao, Chuan-Zhen, Lu
• Format: Article
• Language: English
• Subjects: Animals; Antigens, CD34 - metabolism; Antimetabolites - pharmacology; Behavior, Animal - drug effects; Biological and medical sciences; Brain - pathology; Brain - ultrastructure; Bromodeoxyuridine - pharmacology; Cell Death - physiology; Cell Survival - drug effects; Cerebral Infarction - pathology; Fibronectin; Fibronectins - biosynthesis; Fibronectins - physiology; Genes, bcl-2; Glial Fibrillary Acidic Protein - metabolism; Glucose - deficiency; Granulocyte colony-stimulating factor; Granulocyte Colony-Stimulating Factor - pharmacology; Hippocampal slices; Hippocampus - pathology; Hippocampus - ultrastructure; Hypoxia, Brain - pathology; Immunohistochemistry; Ischemic Attack, Transient - pathology; Ischemic Attack, Transient - prevention & control; Male; Medical sciences; Microscopy, Electron; Middle cerebral artery occlusion; Neurology; Neurons - pathology; Neurons - physiology; Neurons - ultrastructure; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Stem Cells - physiology; Stem Cells - ultrastructure; Survival Analysis; Up-Regulation - physiology; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2006.02.140

Stroke is one of the leading causes of unnatural death and disability. No effective therapy is available. Recombinant human granulocyte colony-stimulating factor (rhG-CSF), as a mobilizing agent for bone marrow stem cells, can promote stem cell mobilization, homing to brain after cerebral ischemia. In the present study, the administration of G-CSF significantly increased number of CD34 + cells in the marginal zone of the infarction. Rats receiving G-CSF had higher survival rate and lower infarction volume. Neurological behavior was improved, and the expression of fibronectin in the ischemic brain was increased, as compared to rats treated with vehicle. To mimic the ischemia–reperfusion injury in experimental animals, we employed hippocampal slice cultures that were first treated with oxygen and glucose deprivation (OGD) and then with oxygen–glucose resupply, finding that fibronectin significantly increased the neurite outgrowth of OGD hippocampal slices, upregulated the expression of Bcl-2 protein, and ameliorated the ultrastructure damage of OGD hippocampal slices.