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Human neural stem cells improve sensorimotor deficits in the adult rat brain with experimental focal ischemia.

Authors
Chu, K; Kim, M; Park, KI; Jeong, SW; Park, HK; Jung, KH; Lee, ST; Kang, L; Lee, K; Park, DK; Kim, SU; Roh, JK
Citation
Brain research, 1016(2):145-153, 2004
Journal Title
Brain research
ISSN
0006-89931872-6240
Abstract
Ischemic stroke is caused by the interruption of cerebral blood flow that leads to brain damage with long-term sensorimotor deficits. Stem cell transplantation may recover functional deficit by replacing damaged brain. In this study, we attempted to test whether the human neural stem cells (NSCs) can improve the outcome in the rat brain with intravenous injection and also determine the migration, differentiation and the long-term viabilities of human NSCs in the rat brain. Focal cerebral ischemia was induced by intraluminal thread occlusion of middle cerebral artery (MCA). One day after surgery, the rats were randomly divided into two groups: NSCs-ischemia vs. Ischemia-only. Human NSCs infected with retroviral vector encoding beta galactosidase were intravenously injected in NSCs-ischemia group (5 x 10(6) cells) and the same amount of saline was injected in Ischemia-only group for control. The animals were evaluated for 4 weeks using turning in an alley (TIA) test, modified limb placing test (MLPT) and rotarod test. Transplanted cells were detected by X gal cytohistochemistry or beta gal immunohistochemistry with double labeling of other cell markers. The NSCs-ischemia group showed better performance on TIA test at 2 weeks, and MLPT and rotarod test from 3 weeks after ischemia compared with the Ischemia-only group. Human NSCs were detected in the lesion side and labeled with marker for neurons or astrocytes. Postischemic hemispheric atrophy was noted but reduced in NSCs-ischemia group. X gal+ cells were detected in the rat brain as long as 540 days after transplantation. Our data suggest intravenously transplanted human NSCs can migrate and differentiate in the rat brain with focal ischemia and improve functional recovery.
MeSH terms
AnimalsBehavior, AnimalBrain Ischemia/*etiology/metabolism/surgeryCell Count/methodsCell Differentiation/drug effectsCells, CulturedDisease Models, AnimalEmbryo, MammalianFunctional Laterality/physiologyGalactosides/diagnostic useGlial Fibrillary Acidic Protein/metabolismHumansImmunohistochemistry/methodsIndoles/diagnostic useInfarction, Middle Cerebral Artery/complications/metabolism/surgeryMaleMicroscopy, Electron/methodsMotor Activity/*physiologyNeurons/cytology/*transplantation/ultrastructurePhosphopyruvate Hydratase/metabolismPsychomotor Performance/physiologyRatsRats, Sprague-DawleyRecovery of FunctionRotarod Performance Test/methodsSensation Disorders/etiology/surgery/*therapyStem Cell Transplantation/*methodsTime FactorsVimentin/metabolism
DOI
10.1016/j.brainres.2004.04.038
PMID
15246850
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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