Archived
This content is available here strictly for research, reference, and/or recordkeeping and as such it may not be fully accessible. If you work or study at University of Kentucky and would like to request an accessible version, please use the SensusAccess Document Converter.
Abstract
BACKGROUND: Accumulation of β-amyloid peptides is an important hallmark of Alzheimer's disease (AD). Tremendous efforts have been directed to elucidate the mechanisms of β-amyloid peptides degradation and develop strategies to remove β-amyloid accumulation. In this study, we demonstrated that a subpopulation of oligodendroglial precursor cells, also called NG2 cells, were a new cell type that can clear β-amyloid peptides in the AD transgene mice and in NG2 cell line.
RESULTS: NG2 cells were recruited and clustered around the amyloid plaque in the APPswe/PS1dE9 mice, which is Alzheimer's disease mouse model. In vitro, NG2 cell line and primary NG2 cells engulfed β-amyloid peptides through the mechanisms of endocytosis in a time dependent manner. Endocytosis is divided into pinocytosis and phagocytosis. Aβ(42) internalization by NG2 cells was mediated by actin-dependent macropinocytosis. The presence of β-amyloid peptides stimulated the autophagic pathway in NG2 cells. Once inside the cells, the β-amyloid peptides in NG2 cells were transported to lysosomes and degraded by autophagy.
CONCLUSIONS: Our findings suggest that NG2 cells are a new cell type that can clear β-amyloid peptides through endocytosis and autophagy.
Document Type
Article
Publication Date
8-10-2013
Digital Object Identifier (DOI)
http://dx.doi.org/10.1186/1750-1326-8-27
Repository Citation
Li, Wenxia; Tang, Yifen; Fan, Zhiqin; Meng, Ya; Yang, Guang; Luo, Jia; and Ke, Zun-Ji, "Autophagy is involved in oligodendroglial precursor-mediated clearance of amyloid peptide" (2013). Internal Medicine Faculty Publications. 10.
https://uknowledge.uky.edu/internalmedicine_facpub/10
Notes/Citation Information
Published in Molecular Neurodegeneration, v. 8, no. 27.
© 2013 Li et al.; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.