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Acute injury directs the migration, proliferation, and differentiation of solid organ stem cells: Evidence from the effect of hypoxia–ischemia in the CNS on clonal “reporter” neural stem cells

Authors
 Kook In Park  ;  Michael A. Hack  ;  Jitka Ourednik  ;  Booma Yandava  ;  Jonathan D. Flax  ;  Philip E. Stieg  ;  Stephen Gullans  ;  Francis E. Jensen  ;  Richard L. Sidmanb  ;  Vaclav Ourednik  ;  Evan Y. Snyder 
Citation
 EXPERIMENTAL NEUROLOGY, Vol.199(1) : 156-178, 2006 
Journal Title
 EXPERIMENTAL NEUROLOGY 
ISSN
 0014-4886 
Issue Date
2006
MeSH
Animals ; Animals, Newborn ; Apoptosis/genetics ; Bromodeoxyuridine/metabolism ; Cell Count/methods ; Cell Differentiation/physiology* ; Cell Movement/physiology* ; Cell Proliferation* ; Clone Cells ; Functional Laterality ; Gene Expression Profiling/methods ; Genes, Reporter/physiology ; Genes, cdc/physiology ; Hypoxia-Ischemia, Brain/physiopathology* ; Hypoxia-Ischemia, Brain/surgery ; Mice ; Microscopy, Electron, Transmission/methods ; Neurons/physiology* ; Neurons/ultrastructure ; Oligonucleotide Array Sequence Analysis/methods ; Stem Cell Transplantation/methods ; Stem Cells/physiology* ; Stem Cells/ultrastructure ; Time Factors
Keywords
Neural stem cells ; Neural injury and degeneration ; Stroke ; Transplantation ; Gene expression ; Development ; Reporter cells
Abstract
Clonal neural cells with stem-like features integrate appropriately into the developing and degenerating central and peripheral nervous system throughout the neuraxis. In response to hypoxic–ischemic (HI) injury, previously engrafted, integrated, and quiescent clonal neural stem cells (NSCs) transiently re-enter the cell cycle, migrate preferentially to the site of ischemia, and differentiate into neurons and oligodendrocytes, the neural cell types typically lost following HI brain injury. They also replenish the supply of immature uncommitted resident stem/progenitor cells. Although they yield astrocytes, scarring is inhibited. These responses appear to occur most robustly within a 3–7 day “window” following HI during which signals are elaborated that upregulate genetic programs within the NSC that mediate proliferation, migration, survival, and differentiation, most of which appear to be terminated once the “window closes” and the chronic phase ensues, sending the NSCs into a quiescent state. These insights derived from using the stem cell in a novel role – as a “reporter” cell – to both track and probe the activity of endogenous stem cells as well as to “interrogate” and “report” the genes differentially induced by the acutely vs. chronically injured milieu. NSCs may be capable of the replacement of cells, genes, and non-diffusible factors in both a widespread or more circumscribed manner (depending on the therapeutic demands of the clinical situation). They may be uniquely responsive to some types of neurodegenerative conditions. We submit that these various capabilities are simply the normal expression of the basic homeostasis-preserving biologic properties and attributes of a stem cell which, if used rationally and in concert with this biology, may be exploited for therapeutic ends.
Full Text
http://www.sciencedirect.com/science/article/pii/S0014488606002366
DOI
10.1016/j.expneurol.2006.04.002
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아청소년과학교실) > 1. Journal Papers
Yonsei Authors
Park, Kook In(박국인) ORCID logo https://orcid.org/0000-0001-8499-9293
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/109075
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