Induction of striatal neurogenesis and generation of region-specific functional mature neurons after ischemia by growth factors

Yoshikawa, Gakushi; Momiyama, Toshihiko; Oya, Soichi; Takai, Keisuke; Tanaka, Junichi; Higashiyama, Shigeki; Saito, Nobuhito; Kirino, Takaaki; Kawahara, Nobutaka

doi:10.3171/2010.2.jns09989

Cited by 35 publications

(27 citation statements)

References 59 publications

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“…52 Our work examines, for the first time, the effects of METH on the pool of SVZ stem/progenitor cells, because these cells have been shown, at least in rodents, to participate in repair programs following brain injury. 15,17,18 Our results, in spite of being obtained from newborn mice SVZ cells, can be translated to adult brain stem cells because the intrinsic capacities of these cells have been shown to be maintained despite aging. 53 Consistently, cocaine administration to adult rodents decreases cell proliferation in the SGZ and SVZ, 20 suggesting that SVZ stem/ progenitor cells display similar sensitivity to drug of abuse throughout life.…”

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confidence: 54%

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Methamphetamine Exerts Toxic Effects on Subventricular Zone Stem/Progenitor Cells and Inhibits Neuronal Differentiation

Bento

Baptista²,

Malva³

et al. 2011

Rejuvenation Research

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Methamphetamine (METH) is a potent and widely consumed psychostimulant drug that causes brain functional and structural abnormalities. However, there is little information regarding METH impact on adult neurogenic niches and, indeed, nothing is known about its consequences on the subventricular zone (SVZ). Thus, this work aims to clarify the effect of METH on SVZ stem/progenitor cells dynamics and neurogenesis. For that purpose, SVZ neurospheres were obtained from early postnatal mice and treated with increasing concentrations of METH (1 μM to 500 μM). Exposure to 100, 250, or 500 μM METH for 24 h triggered cell death both by necrosis and apoptosis, as assessed by propidium iodide uptake, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and quantification of the proapoptotic caspase-3 activity. Furthermore, we showed that METH inhibited SVZ progenitor cells proliferation as it decreased BrdU incorporation. Interestingly, at non-toxic concentrations (1 and 10 μM), METH decreased neuronal differentiation and maturation, which were evaluated by quantification of the number of neuronal nuclei-positive neurons and measurements of phospho-c-Jun-NH(2)-terminal kinase signal in growing axons, respectively. Altogether, our data demonstrate that METH has a negative impact on SVZ stem/progenitor cells, inducing cell death and inhibiting neurogenesis, effects that in vivo may challenge the cell replacement capacities displayed by endogenous populations of brain stem/progenitor cells.

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confidence: 54%

“…12,13 Interestingly, SVZ neurogenesis in rodents is altered in the damaged brain (mainly increased) and provides surrogate neurons with the capacity to reach injured areas. [14][15][16][17][18] Therefore, the SVZ may represent a potential source of cells for brain repair.…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine Exerts Toxic Effects on Subventricular Zone Stem/Progenitor Cells and Inhibits Neuronal Differentiation

Bento

Baptista²,

Malva³

et al. 2011

Rejuvenation Research

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“…Ara-C is a pyrimidine antimetabolite that prevents cell proliferation by inhibiting DNA synthesis. Ara-C has been widely used to inhibit neurogenesis in vivo (Doetsch et al, 1999; Im et al, 2010; Li et al, 2010; Yau et al, 2011; Yoshikawa et al, 2010; Zhang et al, 2004b). Our data show that delayed EPO treatment in the TBI+EPO+Sal group significantly reduces the number of GFAP-positive astrocytes and CD68-positive microglia/macrophages in the DG after TBI as compared to the TBI+Sal+Sal group, indicating the anti-inflammatory effect of EPO (Villa et al, 2003; Yatsiv et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Impact of inhibition of erythropoietin treatment-mediated neurogenesis in the dentate gyrus of the hippocampus on restoration of spatial learning after traumatic brain injury

Zhang

Chopp

Mahmood

et al. 2012

Experimental Neurology

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Our previous study demonstrates that delayed (initiated 24 hours post injury) erythropoietin (EPO) therapy for traumatic brain injury (TBI) significantly improves spatial learning. In this study, we investigated the impact of inhibition of EPO treatment-mediated neurogenesis on spatial learning after experimental TBI. Young male Wistar rats (318±7g) were subjected to unilateral controlled cortical impact injury. TBI rats received delayed EPO treatment (5,000 U/kg in saline) administered intraperitoneally once daily at 1, 2, and 3 days post injury and intracerebroventricular (icv) infusion of either a mitotic inhibitor cytosine-b-D-arabinofuranoside or vehicle (saline) for 14 days. Another 2 groups of TBI rats were treated intraperitoneally with saline and infused icv with either a mitotic inhibitor Ara-C or saline for 14 days. Animals receiving sham operation were infused icv with either Ara-C infusion or saline. Bromodeoxyuridine (BrdU) was administered to label dividing cells. Spatial learning was assessed using a modified Morris water maze test. Animals were sacrificed at 35 days after injury and brain sections stained for immunohistochemical analyses. As compared to the saline treatment, immunohistochemical analysis revealed that delayed EPO treatment significantly increased the number of BrdU-positive cells and new neurons co-stained with BrdU and NeuN (mature neuron marker) in the dentate gyrus in TBI rats. EPO treatment improved spatial learning after TBI. Ara-C infusion significantly abolished neurogenesis and spatial learning recovery after TBI and EPO treatment. Both EPO and Ara-C reduced the number of astrocytes and microglia/macrophages in the dentate gyrus after TBI. Our findings are highly suggestive for an important role of EPO-amplified dentate gyrus neurogenesis as one of the mechanisms underlying EPO therapeutic treatments after TBI, strongly indicating that strategies promoting endogenous neurogenesis may hold an important therapeutic potential for treatment of TBI.

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“…The neuroblasts generated in the V-SVZ migrate toward the injured area and differentiate into functional mature neurons (Yamashita et al, 2006; Kojima et al, 2010; Yoshikawa et al, 2010). …”

Section: Production Of Neuronal and Oligodendrocyte Progenitors In Thmentioning

confidence: 99%

Enhancement of ventricular-subventricular zone-derived neurogenesis and oligodendrogenesis by erythropoietin and its derivatives

Kaneko

Kako

Sawamoto

2013

Front. Cell. Neurosci.

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In the postnatal mammalian brain, stem cells in the ventricular-subventricular zone (V-SVZ) continuously generate neuronal and glial cells throughout life. Genetic labeling of cells of specific lineages have demonstrated that the V-SVZ is an important source of the neuroblasts and/or oligodendrocyte progenitor cells (OPCs) that migrate toward injured brain areas in response to several types of insult, including ischemia and demyelinating diseases. However, this spontaneous regeneration is insufficient for complete structural and functional restoration of the injured brain, so interventions to enhance these processes are sought for clinical applications. Erythropoietin (EPO), a clinically applied erythropoietic factor, is reported to have cytoprotective effects in various kinds of insult in the central nervous system. Moreover, recent studies suggest that EPO promotes the V-SVZ-derived neurogenesis and oligodendrogenesis. EPO increases the proliferation of progenitors in the V-SVZ and/or the migration and differentiation of their progenies in and around injured areas, depending on the dosage, timing, and duration of treatment, as well as the type of animal model used. On the other hand, EPO has undesirable side effects, including thrombotic complications. We recently demonstrated that a 2-week treatment with the EPO derivative asialo-EPO promotes the differentiation of V-SVZ-derived OPCs into myelin-forming mature oligodendrocytes in the injured white matter of neonatal mice without causing erythropoiesis. Here we present an overview of the multifaceted effects of EPO and its derivatives in the V-SVZ and discuss the possible applications of these molecules in regenerative medicine.

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Induction of striatal neurogenesis and generation of region-specific functional mature neurons after ischemia by growth factors

Cited by 35 publications

References 59 publications

Methamphetamine Exerts Toxic Effects on Subventricular Zone Stem/Progenitor Cells and Inhibits Neuronal Differentiation

Methamphetamine Exerts Toxic Effects on Subventricular Zone Stem/Progenitor Cells and Inhibits Neuronal Differentiation

Impact of inhibition of erythropoietin treatment-mediated neurogenesis in the dentate gyrus of the hippocampus on restoration of spatial learning after traumatic brain injury

Enhancement of ventricular-subventricular zone-derived neurogenesis and oligodendrogenesis by erythropoietin and its derivatives

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