Administration of human peripheral blood-derived CD133+ cells accelerates functional recovery in a rat spinal cord injury model.
METHODS
Magnetically isolated, peripheral blood-derived CD133+ cells were used as the therapeutic agent of spinal cord injury (SCI). A rat model was used to investigate the hypothesis that the cell therapy using this clinically accessible cell fraction could be an attractive option for injured spinal cord.


OBJECTIVE
Given the capacity for the peripheral blood-derived CD133+ cells in vivo to produce neurogenesis via vasculogenesis as the feasible candidate for SCI in the clinical setting, the focus of the experiment was to investigate whether the cells could contribute to histologic and functional recovery of SCI after transplantation.


BACKGROUND
No evidence for peripheral blood-derived CD133+ cells application to SCI and no experimental studies showed functional recovery from SCI using this cell fraction have been published.


METHODS
Contusion SCI was induced by placing a 25-g rod onto the spinal cord for 90 seconds in athymic nude rats. CD133+ cells or phosphate-buffered saline was administered intravenously immediately after SCI. The animals were analyzed at specific times after transplantation by several methods to examine histologic vasculogenesis and neurogenesis and to confirm functional recovery from SCI.


RESULTS
After cell transplantation, intrinsic angiogenesis and axonal regeneration were enhanced, and cavity formation was reduced in injured spinal cord, histologically, with significant functional recovery. Gene expression of vascular endothelial growth factor increased in the cell-administrated group.


CONCLUSIONS
The administration of CD133+ cells has a therapeutic potential to a rat spinal cord injury model and could be an optional treatment for spinal cord injury in the clinical settings.
Sasaki
Hirofumi
H
Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Ishikawa
Masakazu
M
Tanaka
Nobuhiro
N
Nakanishi
Kazuyoshi
K
Kamei
Naosuke
N
Asahara
Takayuki
T
Ochi
Mitsuo
M
D000071916:AC133 Antigen; D000818:Animals; D015703:Antigens, CD / Q000032:analysis*; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000276:immunology / Q000378:metabolism / Q000637:transplantation*; D006023:Glycoproteins / Q000032:analysis*; D006085:Graft Survival / Q000502:physiology; D018380:Hematopoietic Stem Cell Transplantation; D006412:Hematopoietic Stem Cells / Q000276:immunology / Q000378:metabolism; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology; D009416:Nerve Regeneration / Q000502:physiology; D055495:Neurogenesis / Q000502:physiology; D010455:Peptides / Q000032:analysis*; D051381:Rats; D011923:Rats, Nude; D020127:Recovery of Function / Q000502:physiology; D013119:Spinal Cord Injuries / Q000503:physiopathology / Q000628:therapy*; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D000071916:AC133 Antigen; D015703:Antigens, CD; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; C000606025:Prom1 protein, rat; D042461:Vascular Endothelial Growth Factor A