Characterization of cells with proliferative activity after a brain injury

Tatsumi, Kouko; Haga, Satomi; Matsuyoshi, Hiroko; Inoue, Masahide; Manabe, Takayuki; Makinodan, Manabu; Wanaka, Akio

doi:10.1016/j.neuint.2004.12.007

Cited by 60 publications

(52 citation statements)

References 25 publications

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“…In contrast, at 3 dpr almost all the GFAP + cells in the ischemic core were degenerated ( Figure 1G), as described elsewhere (Nakagomi et al, 2009), and very few GFAP + / BrdU + cells were found only in the basal ganglia. This finding is in accordance with previous reports dealing with traumatic brain lesions (Tatsumi et al, 2005).…”

Section: Resultssupporting

confidence: 94%

Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Smirkin

Matsumoto

Takahashi

et al. 2009

J Cereb Blood Flow Metab

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In a transient 90-min middle cerebral artery occlusion (MCAO) model of rats, a large ischemic lesion is formed where macrophage-like cells massively accumulate, many of which express a macrophage marker, Iba1, and an oligodendrocyte progenitor cell marker, NG2 chondroitin sulfate proteoglycan (NG2); therefore, the cells were termed BINCs (Brain Iba1 + /NG2 + Cells). A bone marrow transplantation experiment using green-fluorescent protein-transgenic rats showed that BINCs were derived from bone marrow. 5-Fluorouracil (5FU) injection at 2 days post reperfusion (2 dpr) markedly reduced the number of BINCs at 7 dpr, causing enlargement of necrotic volumes and frequent death of the rats. When isolated BINCs were transplanted into 5FU-aggravated ischemic lesion, the volume of the lesion was much reduced. Quantitative real-time RT-PCR showed that BINCs expressed mRNAs encoding bFGF, BMP2, BMP4, BMP7, GDNF, HGF, IGF-1, PDGF-A, and VEGF. In particular, BINCs expressed IGF-1 mRNA at a very high level. Immunohistochemical staining showed that IGF-1-expressing BINCs were found not only in rat but also human ischemic brain lesions. These results suggest that bone marrow-derived BINCs play a beneficial role in ischemic brain lesions, at least in part, through secretion of neuroprotective factors.

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Section: Resultssupporting

confidence: 94%

Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Smirkin

Matsumoto

Takahashi

et al. 2009

J Cereb Blood Flow Metab

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show abstract

“…1N-P and 4, respectively) in agreement with other studies (Herrmann et al, 2000;Yasuda et al, 2004;Tatsumi et al, 2005) may correspond to activated astrocytes after ischemic insult. But although it is accepted that glial cells are activated after brain ischemia, also it is known that multipotent neural precursors have astrocytic morphology and express GFAP, i.e., that GFAP labelling may also correspond to adult neural stem cells (Sun et al, 2003;Alvarez-Buylla and Lim, 2004;Brazel and Rao, 2004;PicardRiera et al, 2004;Steiner et al, 2004;Ming and Song, 2005).…”

Section: Discussionsupporting

confidence: 92%

Ischemia induces cell proliferation and neurogenesis in the gerbil hippocampus in response to neuronal death

Salazar-Colocho

Lanciego

Rı́o

et al. 2008

Neuroscience Research

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We studied hippocampal cellular proliferation and neurogenesis processes in a model of transient global cerebral ischemia in gerbils by labelling dividing cells with 5 0 -Bromo-2 0 -deoxyuridine (BrdU). Surrounding the region of selective neuronal death (CA1 pyramidal layer of the hippocampus), an important increase in reactive astrocytes and BrdU-labelled cells was detected 5 days after ischemia. A similar result was found in the dentate gyrus (DG) 12 days after ischemia. The differentiation of the BrdU+ cells was investigated 28 days after BrdU administration by analyzing the morphology, anatomic localization and cell phenotype by triple fluorescent labelling (BrdU, adult neural marker NeuN and DNA marker TOPRO-3) using confocal laser-scanning microscopy. This analysis showed increased neurogenesis in the DG in case of ischemia and triple positive labelling in some newborn cells in CA1. Seven brain hemispheres from gerbils subjected to ischemia did not develop CA1 neuronal death; hippocampus from these hemispheres did not show any of the above mentioned findings. Our results indicate that ischemia triggers proliferation in CA1 and neurogenesis in the DG in response to CA1 pyramidal neuronal death, independently of the reduced cerebral blood flow or the cell migration from subventricular zone (SVZ). #

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“…Astrocytes produce neurocan, phosphacan and brevican, microglia/macrophages produce NG2 and OPCs produce neurocan, NG2 and versican (Fawcett & Asher 1999;Tang et al 2003;Hampton et al 2004;Properzi & Fawcett 2004;Tatsumi et al 2005). It has recently been suggested that part of NG2-positive cells proliferating in the injury site differentiate into the glial scar astrocytes (Alonso 2005;Tatsumi et al 2005). The CSPGs and other glial scar-associated inhibitory molecules create an environment that blocks the regrowth of neural processes and may potentially cause the exclusion of neural cells by their presence.…”

Section: Factors Affecting Tissue Reaction To the Implanted Neural Elmentioning

confidence: 99%

Biomaterials for the central nervous system

Zhong

Bellamkonda

2008

J. R. Soc. Interface.

215

163

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Biomaterials are widely used to help treat neurological disorders and/or improve functional recovery in the central nervous system (CNS). This article reviews the application of biomaterials in (i) shunting systems for hydrocephalus, (ii) cortical neural prosthetics, (iii) drug delivery in the CNS, (iv) hydrogel scaffolds for CNS repair, and (v) neural stem cell encapsulation for neurotrauma. The biological and material requirements for the biomaterials in these applications are discussed. The difficulties that the biomaterials might face in each application and the possible solutions are also reviewed in this article.

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Characterization of cells with proliferative activity after a brain injury

Cited by 60 publications

References 25 publications

Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Ischemia induces cell proliferation and neurogenesis in the gerbil hippocampus in response to neuronal death

Biomaterials for the central nervous system

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Characterization of cells with proliferative activity after a brain injury

Cited by 60 publications

References 25 publications

Iba1+/NG2+ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Iba1+/NG2+ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Ischemia induces cell proliferation and neurogenesis in the gerbil hippocampus in response to neuronal death

Biomaterials for the central nervous system

Contact Info

Product

Resources

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Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain

Iba1⁺/NG2⁺ Macrophage-Like Cells Expressing a Variety of Neuroprotective Factors Ameliorate Ischemic Damage of the Brain