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Neural Stem Cells and Oligodendrocyte Progenitors in the Central Nervous System
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Jennifer A. Jackson, Diana L. Clarke
When glioblast formation ceases shortly after birth, the germinal VZ disappears throughout the neuroaxis and many of the remaining neuroepithelial cells become ependymal cells. The ependymal cells persist throughout adulthood lining the luminal surface of the ventricular system of the brain and the central canal of the spinal cord. These cells possess multiple cilia on their apical surface that effectively move the cerebral spinal fluid throughout these regions. Similarly, the SVZ, decreases in size and persists immediately adjacent to the ependymal cell layer throughout most of the ventricular regions of the brain. However, a SVZ region is not present in the developing or mature regions of the spinal cord.
Cadmium induces CCL2 production in glioblastoma cells via activation of MAPK, PI3K, and PKC pathways
Published in Journal of Immunotoxicology, 2020
Thitima Kasemsuk, Suttinee Phuagkhaopong, Ruedeemars Yubolphan, Norapat Rungreangplangkool, Pornpun Vivithanaporn
High levels of CCL2 lead to increased leukocyte infiltration into CNS and subsequently cause neuroinflammation. The up-regulation of CCL2 triggered IL-6 expression, migration, and invasion of U-87 MG (Lindemann et al. 2015; Zhang et al. 2012). A Cd-induced CCL2 expression together with an induction of IL-6 and IL-8 from glioblastoma cells could facilitate the infiltration of microglia/macrophages into tumors and associated tissues, and enhance the migration and invasion of glioblastoma cells, leading to greater deleterious effects. The production of CCL2 by tumor-associated macrophages during cases of glioblastoma triggered an infiltration of regulatory T-cells and myeloid-derived suppressor cells, resulting in local immunosuppression (Chang et al. 2016). Therefore, increases in CCL2 expression by glioblast-omas that are caused by Cd could be one of many factors that could contribute to overall cancers or glioblastomas in particular due to exposure to this metal.
Vulnerability of glia and vessels of rat substantia nigra in rotenone Parkinson model
Published in Ultrastructural Pathology, 2018
Sanaa A. M. Elgayar, Amel A. M. Abdel-hafez, Asmaa M. S. Gomaa, Raghda Elsherif
The astrocytes increased in number and they were encountered in contiguous pairs which indicate proliferation. The reactive astrocytes revealed conformational changes and occasionally dense cytoplasm. They exhibited cytological features of immature astrocyte or glioblast; irregular large nuclei relative to the cytoplasm with numerous heterochromatin clumps, a few RER segments, filaments and glycogen; and occasionally centrioles.22 These findings correlate with the increase of the astrocyte number (proliferation). It is reported that certain mature astrocytes exposed to central nervous system injury resume the properties of earlier developmental stages, along with acquisition of stem cell properties,23 which lends support to our suggestion. The source of newly divided astrocytes may include mature astrocytes that re-enter the cell cycle.23 Interestingly, it is suggested that the remodeling process is independently regulated through a reactive oxygen species (ROS)-signaling mechanism.41