Vascular Endothelial Growth Factor Directly Inhibits Primitive Neural Stem Cell Survival But Promotes Definitive Neural Stem Cell Survival

Wada, Tamaki; Haigh, Jody J.; Ema, Masatsugu; Hitoshi, Seiji; Chaddah, Radha; Rossant, Janet; Nagy, András; Kooy, Derek van der

doi:10.1523/jneurosci.0526-06.2006

Cited by 94 publications

(79 citation statements)

References 43 publications

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“…Few NSCs were growing in the vehicle conditions, whereas NSCs were more abundant after ALA treatment (Figure 2b). This observation was confirmed by immunohistochemistry using Ki-67 nuclear protein staining, the expression of which is strictly associated with cell proliferation and is routinely used as a proliferation marker (Wada et al, 2006;Maysami et al, 2008). Indeed, after 3 days of ALA treatment, a nearly 1.6-fold increase in the percentage of Ki-67-positive NSCs was seen (36.5 ± 2.9% of Ki-67-positve NSCs reached 58.1±3.3% in presence of 100 mM ALA, po0.001), clearly indicating an increase in cell division and marked NSC proliferation (Figure 3c, right panel).…”

Section: Ala Treatment Triggers In Vitro Bdnf Expression and Promotesmentioning

confidence: 73%

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Blondeau

Nguemeni

Debruyne

et al. 2009

Neuropsychopharmacol

122

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Omega-3 polyunsaturated fatty acids are known to have therapeutic potential in several neurological and psychiatric disorders. However, the molecular mechanisms of action underlying these effects are not well elucidated. We previously showed that alpha-linolenic acid (ALA) reduced ischemic brain damage after a single treatment. To follow-up this finding, we investigated whether subchronic ALA treatment promoted neuronal plasticity. Three sequential injections with a neuroprotective dose of ALA increased neurogenesis and expression of key proteins involved in synaptic functions, namely, synaptophysin-1, VAMP-2, and SNAP-25, as well as proteins supporting glutamatergic neurotransmission, namely, V-GLUT1 and V-GLUT2. These effects were correlated with an increase in brain-derived neurotrophic factor (BDNF) protein levels, both in vitro using neural stem cells and hippocampal cultures and in vivo, after subchronic ALA treatment. Given that BDNF has antidepressant activity, this led us to test whether subchronic ALA treatment could produce antidepressant-like behavior. ALA-treated mice had significantly reduced measures of depressive-like behavior compared with vehicletreated animals, suggesting another aspect of ALA treatment that could stimulate functional stroke recovery by potentially combining acute neuroprotection with long-term repair/compensatory plasticity. Indeed, three sequential injections of ALA enhanced protection, either as a pretreatment, wherein it reduced post-ischemic infarct volume 24 h after a 1-hour occlusion of the middle cerebral artery or as post-treatment therapy, wherein it augmented animal survival rates by threefold 10 days after ischemia.

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Section: Ala Treatment Triggers In Vitro Bdnf Expression and Promotesmentioning

confidence: 73%

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Blondeau

Nguemeni

Debruyne

et al. 2009

Neuropsychopharmacol

122

View full text Add to dashboard Cite

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“…VEGF is reported to stimulate adult neurogenesis in vivo (20,21) and proliferation of brain-derived neural stem/progenitor cells in vitro (22,23). We have reported that VEGF-Flk-1 signaling underlies ECS induction of hippocampal cell proliferation (17) and importantly, rescues hippocampal cell proliferation after irradiation exposure (24).…”

Section: Discussionmentioning

confidence: 97%

Electroconvulsive seizure and VEGF increase the proliferation of neural stem-like cells in rat hippocampus

Segi-Nishida

Warner-Schmidt

Duman

2008

Proc. Natl. Acad. Sci. U.S.A.

206

149

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All classes of antidepressants increase hippocampal cell proliferation and neurogenesis, which contributes, in part, to the behavioral actions of these treatments. Among antidepressant treatments, electroconvulsive seizure (ECS) is the most robust stimulator of hippocampal cell proliferation and the most efficacious treatment for depression, but the cellular mechanisms underlying the actions of ECS are unknown. To address this question, we investigated the effect of ECS on proliferation of neural stem-like and/or progenitor cells in the subgranular zone of rat dentate gyrus. We define the neural differentiation cascade from stem-like cells to early neural progenitors (also referred to as quiescent and amplifying neural progenitors, respectively) by coexpression of selective cellular and mitotic activity markers. We find that at an early mitotic phase ECS increases the proliferation of quiescent progenitors and then at a later phase increases the proliferation of amplifying progenitors. We further demonstrate that vascular endothelial growth factor (VEGF) signaling is necessary for ECS induction of quiescent neural progenitor cell proliferation and is sufficient to produce this effect. These findings demonstrate that ECS and subsequent induction of VEGF stimulates the proliferation of neural stem-like cells and neural progenitor cells, thereby accounting for the superior neurogenic actions of ECS compared with chemical antidepressants.depression ͉ neurogenesis ͉ antidepressant ͉ neurotrophic factor E lectroconvulsive seizure (ECS) therapy is considered the most effective treatment for depression, including patients who do not respond to chemical antidepressants (1-3). Recent studies demonstrate that all classes of antidepressants increase neurogenesis in the adult hippocampus, and this effect is thought to contribute, in part, to the actions of these treatments in rodent behavioral models (4-6). However, the cellular basis for the antidepressant induction of hippocampal neurogenesis has not been fully characterized. Previous studies have demonstrated that antidepressants, such as ECS and fluoxetine, increase cell proliferation within the subgranular zone (SGZ) and accelerate the maturation of immature neuron of the dentate gyrus in hippocampus but do not affect the differentiation of progenitor cells into neurons or glia (7-10). This indicates that one of the main targets for antidepressant-induced neurogenesis is to increase the mitotic activity of neural progenitor cells in the SGZ.Two major subclasses of proliferating cells have been characterized in the hippocampal SGZ based on the expression of phenotypic marker proteins. The first class is the putative stem cell that has a radial glia-like morphology, characterized by expression of glial fibrillary acidic protein (GFAP) and a relatively low rate of proliferative activity. This cell population is called the neural stem-like cell, type 1 cell, B cell, or quiescent neural progenitor (QNP) (11-13). The second class of cells is GFAP-negative, has a relatively hi...

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“…An increasing number of reports suggest that VEGFA has direct effects on nonvascular cells including neuronal cells (Marti & Risau 1998, Wada et al 2006, Nishijima et al 2007), muscle cells (Germani et al 2003, Bryan et al 2008, and granulosa cells (Greenaway et al 2004). Data also suggest potential functional roles for VEGFA in the postnatal testis, as KDR and FLT1 are expressed in testicular germ cells in humans (Ergun et al 1997), rats (Rudolfsson et al 2004), and mice (Nalbandian et al 2003), while somatic Sertoli and Leydig cells produce VEGFA (Liu & Yang 2004).…”

Section: Introductionmentioning

confidence: 99%

Vascular endothelial growth factor regulates germ cell survival during establishment of spermatogenesis in the bovine testis

Caires

Avila²,

McLean

2009

Reproduction

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Vascular endothelial growth factor-A (VEGFA) is a hypoxia-inducible peptide essential for angiogenesis and targets nonvascular cells in a variety of tissues and cell types. The objective of the current study was to determine the function of VEGF during testis development in bulls. We used an explant tissue culture and treatment approach to test the hypothesis that VEGFA-164 could regulate the biological activity of bovine germ cells. We demonstrate that VEGFA, KDR, and FLT1 proteins are expressed in germ and somatic cells in the bovine testis. Treatment of bovine testis tissue with VEGFA in vitro resulted in significantly more germ cells following 5 days of culture when compared with controls. Quantitative real-time RT-PCR analysis determined that VEGF treatment stimulated an intracellular response that prevents germ cell death in bovine testis tissue explants, as indicated by increased expression of BCL2 relative to BAX and decreased expression of BNIP3 at 3, 6, and 24 h during culture. Blocking VEGF activity in vitro using antisera against KDR and VEGF significantly reduced the number of germ cells in VEGF-treated testis tissue to control levels at 120 h. Testis grafting provided in vivo evidence that bovine testis tissue treated with VEGFA for 5 days in culture contained significantly more differentiating germ cells compared with controls. These findings support the conclusion that VEGF supports germ cell survival and sperm production in bulls.

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Vascular Endothelial Growth Factor Directly Inhibits Primitive Neural Stem Cell Survival But Promotes Definitive Neural Stem Cell Survival

Abstract: There are two types of neural stem cells (NSCs). Primitive NSCs [leukemia inhibitory factor (LIF) dependent but exogenous fibroblast

Cited by 94 publications

References 43 publications

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Electroconvulsive seizure and VEGF increase the proliferation of neural stem-like cells in rat hippocampus

Vascular endothelial growth factor regulates germ cell survival during establishment of spermatogenesis in the bovine testis

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