Cells that express the NG2 proteoglycan (NG2+ cells) comprise a unique population of glial cells in the central nervous system. While there is no question that some NG2+ cells differentiate into oligodendrocytes during development, the persistence of numerous NG2+ cells in the mature CNS has raised questions about their identity, relation to other CNS cell types, and functions besides their progenitor role. NG2+ cells also express the alpha receptor for platelet-derived growth factor (PDGF alphaR), a receptor that mediates oligodendrocyte progenitor proliferation during development. Antigenically, NG2+ cells are distinct from fibrous and protoplasmic astrocytes, resting microglia, and mature oligodendrocytes. Therefore, we propose the term polydendrocytes to refer to all NG2-expressing glial cells in the CNS parenchyma. This distinguishes them from the classical glial cell types and identifies them as the fourth major glial population in the CNS. Recent observations suggest that polydendrocytes are complex cells that physically and functionally interact with other cell types in the CNS. Committed oligodendrocyte progenitor cells arise from restricted foci in the ventral ventricular zone in both spinal cord and brain. It remains to be clarified whether there are multiple sources of oligodendrocytes, and if so whether polydendrocytes (NG2+ cells) represent progenitor cells of all oligodendrocyte lineages. Proliferation of NG2+ cells during early development appears to be dependent on PDGF, but the regulatory mechanisms that govern NG2+ cell proliferation in the mature CNS remain unknown. Pulse-chase labeling with bromodeoxyuridine indicates that polydendrocytes that proliferate in the postnatal spinal cord differentiate into oligodendrocytes. Novel experimental approaches are being developed to further elucidate the functional properties and differentiation potential of polydendrocytes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1023/a:1025783412651 | DOI Listing |
J Transl Med
December 2024
Department of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, 2075 Qunli Seventh Avenue, Daoli District, Harbin, 150001, Heilongjiang Province, China.
Background: Spinal cord injury (SCI) inflicts a severe burden on patients and lacks effective treatments. Owing to the poor regenerative capabilities of endogenous oligodendrocyte precursor cells (OPCs) following SCI, there is a growing interest in alternative sources, such as human umbilical cord mesenchymal stem cells (HUCMSCs). TET3 is a key DNA demethylase that plays an important role in neural differentiation, but its role in OPC formation is not well understood.
View Article and Find Full Text PDFCNS Neurosci Ther
December 2024
Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, NHC Key Laboratory of Chronobiology, Sichuan University, Chengdu, China.
Background: Preterm white matter injury (PWMI) is the most common type of brain injury in preterm infants, in which, oligodendrocyte progenitor cells (OPCs) are predominantly damaged. In this study, human OPCs (hOPCs) were administered to a fetal goat model of PWMI to examine the differentiation potential and therapeutic effects of the cells on PWMI.
Methods: Preterm goat fetuses were subjected to hypoxic-ischemia (HI) via intermittent umbilical cord occlusion (5 min × 5).
Int J Mol Sci
December 2024
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.
Multiple sclerosis (MS) is a chronic neurodegenerative disorder involving demyelination. The cuprizone model is commonly used to study MS by inducing oligodendrocyte stress and demyelination. The subventricular zone (SVZ) plays a key role in neurogenesis, while the neuronal/glial antigen 2 (NG2) is a marker for immature glial cells, involved in oligodendrocyte differentiation.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Ophthalmology, Kansai Medical University, 2-5-1 Shin-machi, Hirakata 573-1010, Osaka, Japan.
Retinopathy of prematurity (ROP) is primarily caused by the exposure of preterm infants with underdeveloped blood vessels to high oxygen concentrations. This damages the astrocytes that promote normal vascular development, leading to avascularity, pathological neovascularization, and retinal detachment, and even blindness as the disease progresses. In this study, the aim was to investigate the differences in the characteristics of astrocytes and blood vessels between wild-type (WT) and genetically modified mice overexpressing platelet-derived growth factor subunit A (PDGF-A) in the retina immediately after high oxygen exposure, a protocol in the oxygen-induced retinopathy (OIR) model of ROP.
View Article and Find Full Text PDFAngiogenesis
December 2024
Department of Pharmaceutical Sciences, Università del Piemonte Orientale, Novara, Italy.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!