title: Increase in bFGF-responsive neural progenitor population following contusion injury of the adult rodent spinal cord.
abstract: The number of neural progenitor cells, especially nestin+ cells or BrdU-uptake cells is sparse in the normal adult rodent spinal cord. However, in the present study, we show that after spinal cord injury (SCI), many ordinarily quiescent cells were activated to become nestin+ and undergo mitosis (BrdU+) in the ependymal layer as well as in the parenchyma of the spinal cord. Nestin+ cells and BrdU+ cells were in most cases immunohistochemically GFAP+, some of which displayed radial glial cell morphology and partly participated in the border formation of the lesion. The culturing of injured rat spinal cord tissues generated more neurospheres earlier than did the culturing of intact tissues, and these neurosphere cells were multipotent and bFGF-responsive. Immunohistochemical analysis showed that there existed many bFGF+ cells after SCI, the number of which were almost 15 times greater than that in an intact spinal cord. Increased bFGF production after SCI might activate quiescent progenitor cells, and thus initiate their cell proliferation. Finally, SCI to the nestin-promoter green fluorescent protein (GFP) transgenic mice showed broad proliferation of progenitor cells that were induced in the injured spinal cord. The culturing of injured spinal cord tissues from these transgenic mice provides direct evidence that neurospheres can be generated by SCI-activated nestin+ cells. Thus, the activation of bFGF-responsive progenitor cells and the concomitant increase in the population of bFGF+ cells following SCI might be beneficial for spinal cord repair if these progenitor cells are properly manipulated.
authors.affiliation: Department of Anatomy and Neurobiology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606 8501, Japan. Yi_Xu@dfci.harvard.edu
authors.forename: Yi
authors.initials: Y
authors.lastname: Xu
authors.forename: Masaaki
authors.initials: M
authors.lastname: Kitada
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Mari
authors.initials: M
authors.lastname: Dezawa
authors.forename: Chizuka
authors.initials: C
authors.lastname: Ide
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D049452:Green Fluorescent Proteins / Q000235:genetics; D007150:Immunohistochemistry; D007381:Intermediate Filament Proteins / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D039902:Multipotent Stem Cells / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics; D064231:Nestin; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D011401:Promoter Regions, Genetic; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology*; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*
chemical_list: D007381:Intermediate Filament Proteins; D009419:Nerve Tissue Proteins; C577485:Nes protein, mouse; C577486:Nes protein, rat; D064231:Nestin; D016222:Fibroblast Growth Factor 2; D049452:Green Fluorescent Proteins