title: Increase of NG2-positive cells associated with radial glia following traumatic spinal cord injury in adult rats.
abstract: In the CSN including the spinal cord, NG2 proteoglycan is a marker of oligodendrocyte progenitors. To elucidate the dynamics of the endogenous neural stem (progenitor) cells in adult rats with spinal cord injury (SCI), we examined an immunohistochemical analysis of NG2, GFAP, and 3CB2, a specific marker of radial glia (RG). SD rats were divided into a SCI group (n = 25) and a sham-operated group (n = 5). In the injury group, laminectomy was performed at Th11-12 and contusive compression injury was created by applying a weight of 30 g for 10 min. Rats were sacrificed at 24 h, and 1, 4, 8 and 12 weeks post-injury. Frozen 20-mu m sections of tissue 5 and 10 mm rostral and caudal to the epicenter of injury were prepared. Immunohistochemistry was performed using antibodies against NG2, GFAP and 3CB2. At 4 weeks after injury, NG2-positive glial cells arose from below the pial surface as bipolar cells with processes extending throughout the entire white matter. NG2 expression peaked at 4 weeks after injury, showing a 7-fold increase compared to the 24 h after injury. The NG2-positive cells with processes which increased in the white matter of the spinal cord were GFAP-positive and also co-localized with 3CB2 antigen. The pattern of NG2 expression of these cells was temporally and spatially different from the pattern of NG2 expression that accumulated around the hemorrhagic and necrotic epicenter. These results suggest that NG2 positive cells which derived from subpial layer, may have some lineage to RG after SCI in adult rodents.
authors.affiliation: Departments of Orthopaedic Surgery, School of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kagawa, 761-0793, Japan.
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.forename: Sei
authors.initials: S
authors.lastname: Shibuya
authors.forename: Osamu
authors.initials: O
authors.lastname: Miyamoto
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Itano
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism*; D000943:Antigens, Differentiation / Q000378:metabolism; D002454:Cell Differentiation / Q000502:physiology; D019070:Cell Lineage / Q000502:physiology; D049109:Cell Proliferation; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D009416:Nerve Regeneration / Q000502:physiology*; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000503:physiopathology; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D000943:Antigens, Differentiation; D005904:Glial Fibrillary Acidic Protein; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4