Neural Stem Cells and Progenitor Cells

The biologic potential of NSCs endows them with the ability to integrate into the neural circuitry after transplantation. The replacement of cells may be specific not only to anatomically circumscribed regions of the brain but also to large areas of the injured central nervous system (16). Primary cultured neurosphere-forming cells (NSCs and NPCs), derived from the SVZ in adult rats, have been employed for the treatment of stroke (17). These cells, also labeled by ferromagnetic particles, were intracisternally transplanted into rats that had been subjected to middle cerebral artery occlusion (MCAO), the major cause of stroke (18). Rats transplanted with SVZ cells exhibited significant improvement of neurologic function. Migration of transplanted cells was noninvasively tracked using magnetic resonance imaging (MRI). Transplanted cells selectively migrated within the central nervous system toward the ischemic parenchyma at a mean speed of 65 ± 14.6 |m/hr. Migration, proliferation, and differentiation of transplanted cells in the brain were also measured histopathologically. Primary cultured human fetal NSCs and NPCs xenografted into the lesioned areas in the brains of Mongolian gerbils after focal ischemia also significantly improved neurologic function. These cells migrate to the infarction, differentiate into mature neurons, and form synapses with host neuronal circuits (19). Thus, these primary cultured neurosphere cells are a potential source for transplantable material for the treatment of stroke and MRI can be used to track grafted cells in the brain.

In rodents, other cell lines that are derived from NSCs and NPCs target and integrate into the central nervous system and migrate to areas of subsequent infarction. For example, murine neonatal neural C17.2 cells, stably transfected with firefly luciferase, were serially imaged through intact skull and skin by bioluminescence imaging in MCAO mice after contralateral intraparenchymal or intraventricular injections (20). The cells migrated to the site of infarct from the contralateral parenchyma, crossing the midline. In control animals without infarcts, C17.2 cells remained at the site of administration. Intraventricular cell administration resulted in a wide distribution of cells, including the site of infarct. Within the infarct area, C17.2 cells colabeled with a neural marker. Images correlated well with histologic cell distributions (20 ). The conditionally immortal Maudsley hippocampal clone 36 (MHP36) NSCs, originally derived from the H-2Kb-tsA58 transgenic mouse, were effective in reversing sensory and motor deficits and in reducing lesion volume as a consequence of MCAO (21). Grafts of the MHP36 cells also repaired cognitive function, reduced lesion volume, and differentiated into site-appropriate phenotypes after global and focal ischemia in rats (22,23 ). MHP36 cells may improve functional outcome after MCAO by assisting spontaneous reorganization in both the damaged and intact hemispheres (24). ReNeuron (Surrey, UK) is currently developing, from different brain regions, human neuroepithelial stem cell lines with similar reparative properties to murine lines (21).

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