NG2 colocalizes with axons and is expressed by a mixed cell population in spinal cord lesions.
The NG2 proteoglycan is of general interest after spinal cord injury because it is expressed by oligodendrocyte progenitors (OPCs), which contribute to central nervous system remyelination; however, NG2 may inhibit axon regeneration. We and others have examined the spatiotemporal expression of NG2 after spinal cord injury (SCI). Here, we extend those observations and provide a comprehensive analysis of the distribution, phenotype, and colocalization of NG2 cells with axons in a clinically relevant model of spinal contusion. Because contusion models mimic the majority of human SCI, this information is important for understanding endogenous processes that promote and/or prevent repair. The data demonstrate that NG2 levels rise significantly between 3 and 7 days postinjury (dpi) and remain elevated chronically throughout the lesions. NG2 within the lesions could be derived from an array of infiltrating cells; thus, a panel of antibodies was used to investigate NG2 cell phenotypes. First, platelet-derived growth factor-alpha receptor (PDGFalphaR) colocalization was examined because OPCs normally express both markers. PDGFalphaR cells were present in lesions at all times examined. However, only 37% of NG2 cells coexpressed PDGFalphaR at 14 dpi, which dropped to <1% by 70 dpi. This contrasts with the nearly complete overlap in spared tissue surrounding the lesion. In contrast, 40% to 60% of NG2 cells expressed p75 and approximately 84% expressed Sox10, suggesting that many NG2 cells were nonmyelinating Schwann cells. Despite rising levels of NG2, we noted robust and sustained axon growth into the lesions, many of which were located along NG2 profiles. Thus, spinal contusion produces an NG2-rich environment into which axons grow and in which the source of NG2 appears considerably different from that in surrounding spared tissue.
McTigue
Dana M
DM
From the Department of Neuroscience and Spinal Trauma and Repair (STAR) Laboratories, Ohio State University, Columbus, Ohio.
Tripathi
Richa
R
Wei
Ping
P
D000818:Animals; D000941:Antigens / Q000096:biosynthesis*; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D009416:Nerve Regeneration / Q000502:physiology*; D016900:Neurofilament Proteins / Q000096:biosynthesis; D009836:Oligodendroglia / Q000166:cytology / Q000378:metabolism; D010641:Phenotype; D011509:Proteoglycans / Q000096:biosynthesis*; D051381:Rats; D011916:Rats, Inbred F344; D017479:Receptors, Platelet-Derived Growth Factor / Q000096:biosynthesis; D012583:Schwann Cells / Q000166:cytology / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology; D000099216:Chondroitin Sulfate Proteoglycan 4
D000941:Antigens; D016900:Neurofilament Proteins; D011509:Proteoglycans; D017479:Receptors, Platelet-Derived Growth Factor; D000099216:Chondroitin Sulfate Proteoglycan 4