Administration of CD34+ cells after stroke enhances neurogenesis via angiogenesis in a mouse model

Thrombo-occlusive cerebrovascular disease resulting in stroke and permanent neuronal loss is an important cause of morbidity and mortality. Because of the unique properties of cerebral vasculature and the limited reparative capability of neuronal tissue, it has been difficult to devise effective neu...

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Bibliographic Details
Published in:The Journal of clinical investigation 2004-08, Vol.114 (3), p.330-338
Main Authors: Taguchi, Akihiko, Soma, Toshihiro, Tanaka, Hidekazu, Kanda, Takayoshi, Nishimura, Hiroyuki, Yoshikawa, Hiroo, Tsukamoto, Yoshitane, Iso, Hiroyuki, Fujimori, Yoshihiro, Stern, David M, Naritomi, Hiroaki, Matsuyama, Tomohiro
Format: Article
Language:English
Subjects:
Animals
Antigens, CD34 - administration & dosage
Antigens, CD34 - immunology
Behavior, Animal
Biomarkers - blood
Cell Division - immunology
Disease Models, Animal
Fetal Blood - cytology
Humans
Immunohistochemistry
Infant, Newborn
Injections, Intravenous
Male
Mice
Mice, Inbred C57BL
Mice, SCID
Neovascularization, Physiologic - immunology
Nerve Tissue Proteins - metabolism
Neurons - immunology
Neurons - physiology
RNA-Binding Proteins - metabolism
Stem Cell Transplantation
Stroke - therapy
Time Factors
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Summary:Thrombo-occlusive cerebrovascular disease resulting in stroke and permanent neuronal loss is an important cause of morbidity and mortality. Because of the unique properties of cerebral vasculature and the limited reparative capability of neuronal tissue, it has been difficult to devise effective neuroprotective therapies in cerebral ischemia. Our results demonstrate that systemic administration of human cord blood-derived CD34(+) cells to immunocompromised mice subjected to stroke 48 hours earlier induces neovascularization in the ischemic zone and provides a favorable environment for neuronal regeneration. Endogenous neurogenesis, suppressed by an antiangiogenic agent, is accelerated as a result of enhanced migration of neuronal progenitor cells to the damaged area, followed by their maturation and functional recovery. Our data suggest an essential role for CD34(+) cells in promoting directly or indirectly an environment conducive to neovascularization of ischemic brain so that neuronal regeneration can proceed.
ISSN:0021-9738
DOI:10.1172/jci200420622