Temporospatial expression and cellular localization of oligodendrocyte myelin glycoprotein (OMgp) after traumatic spinal cord injury in adult rats.
Traumatic spinal cord injury (SCI) leads to permanent neurological deficits, which, in part, is due to the inability of mature axons to regenerate in the mammalian central nervous system (CNS). The oligodendrocyte myelin glycoprotein (OMgp) is one of the myelin-associated inhibitors of neurite outgrowth in the CNS. To date, limited information is available concerning its expression following SCI, possibly due to the lack of a reliable antibody against it. Here we report the generation of a highly specific OMgp polyclonal antibody from the rabbit. Using this antibody, we found that OMgp was almost exclusively expressed in the CNS. Following a moderately contusive SCI using a New York University impactor (10 g rod dropped from a height of 12.5 mm), both OMgp mRNA and protein levels were elevated at 1 and 7 days post-SCI, respectively, and peaked at 28 days compared to those of the sham-operated controls. Spatially, OMgp was expressed throughout the entire rostrocaudal extension of a 10 mm long spinal segment with the highest expression seen at the injury epicenter. OMgp was exclusively localized in neurons and oligodendrocytes in the normal and sham-operated controls with an increased expression found in these cells following SCI. OMgp was not expressed in astrocytes or microglia in all groups. Thus, our study has provided evidence for temporospatial expression and cellular localization of OMgp following SCI and suggested that this molecule may contribute to the overall inhibition of axonal regeneration.
Dou
Fangfang
F
Department of Neurobiology, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Huang
Lidong
L
Yu
Panpan
P
Zhu
Huiqing
H
Wang
Xiaofei
X
Zou
Jian
J
Lu
Peihua
P
Xu
Xiao-Ming
XM
D000818:Animals; D000918:Antibody Specificity; D004195:Disease Models, Animal; D005260:Female; D020439:Growth Cones / Q000378:metabolism; D006131:Growth Inhibitors / Q000378:metabolism; D007150:Immunohistochemistry / Q000379:methods; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein / Q000235:genetics / Q000378:metabolism*; D063308:Myelin-Oligodendrocyte Glycoprotein; D009413:Nerve Fibers, Myelinated / Q000378:metabolism* / Q000473:pathology; D009416:Nerve Regeneration / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology
D006131:Growth Inhibitors; C571328:Mog protein, rat; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein; D063308:Myelin-Oligodendrocyte Glycoprotein; D012333:RNA, Messenger