N-cadherin mediates nitric oxide-induced neurogenesis in young and retired breeder neurospheres

Chen, J.; Zacharek, Alex; Li, Y.; Li, A.; Wang, L.; Katakowski, Mark; Roberts, Cynthia J.; Lü, Mei; Chopp, Michael

doi:10.1016/j.neuroscience.2006.02.064

Cited by 40 publications

(43 citation statements)

References 43 publications

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“…EC-SOD had been shown to control the bioavailability of nitric oxide (NO) within the vascular wall and the lung (30,31). Although similar work had not been performed in the nervous system, it was reasonable to assume that more NO would be available in the OE mice to facilitate dendrite outgrowth (32,33). Because the molecular layer of dentate gyrus was expected to be devoid of EC-SOD (other than the circulating form originating from the granule cells) in OE mice, the observation that the dendrites in OE mice did not reach as far into the molecular layer as that in WT mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation

Zou¹,

Corniola²,

Leu

et al. 2012

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

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Cranial irradiation is widely used in cancer therapy, but it often causes cognitive defects in cancer survivors. Oxidative stress is considered a major cause of tissue injury from irradiation. However, in an earlier study mice deficient in the antioxidant enzyme extracellular superoxide dismutase (EC-SOD KO) showed reduced sensitivity to radiation-induced defects in hippocampal functions. To further dissect the role of EC-SOD in neurogenesis and in response to irradiation, we generated a bigenic EC-SOD mouse model (OE mice) that expressed high levels of EC-SOD in mature neurons in an otherwise EC-SOD-deficient environment. EC-SOD deficiency was associated with reduced progenitor cell proliferation in the subgranular zone of dentate gyrus in KO and OE mice. However, high levels of EC-SOD in the granule cell layer supported normal maturation of newborn neurons in OE mice. Following irradiation, wild-type mice showed reduced hippocampal neurogenesis, reduced dendritic spine densities, and defects in cognitive functions. OE and KO mice, on the other hand, were largely unaffected, and the mice performed normally in neurocognitive tests. Although the resulting hippocampalrelated functions were similar in OE and KO mice following cranial irradiation, molecular analyses suggested that they may be governed by different mechanisms: whereas neurotrophic factors may influence radiation responses in OE mice, dendritic maintenance may be important in the KO environment. Taken together, our data suggest that EC-SOD plays an important role in all stages of hippocampal neurogenesis and its associated cognitive functions, and that highlevel EC-SOD may provide protection against irradiation-related defects in hippocampal functions.

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Section: Discussionmentioning

confidence: 99%

Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation

Zou¹,

Corniola²,

Leu

et al. 2012

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

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“…To examine neural responses to reward anticipation, participants were scanned while performing a modified monetary incentive delay task, which has been shown to induce ventral tion, NOS1 functions in neurite outgrowth, suggesting an early influence on brain development (17).…”

Section: Fu N C Tio N a L M A G N E Tic R E So N A N C E Im A G In G mentioning

confidence: 99%

Nitric Oxide Synthase Genotype Modulation of Impulsivity and Ventral Striatal Activity in Adult ADHD Patients and Healthy Comparison Subjects

Hoogman¹,

Aarts²,

Zwiers³

et al. 2011

AJP

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(5), as evidenced by steeper temporal discounting rates, altered decision making, and an aversion to delay of gratification in reward-related tests (6-9). Temporal discounting is the patient's preference to receive smaller rewards sooner rather than larger rewards later and is postulated to be an intermediate phenotype for impulsivity. Neuroimaging studies have shown engagement of alternative brain regions in decision making in ADHD patients (10). A prominent feature is hypoactivation of the ventral striatum, a brain area with an important role in reward processing (11,12), during reward anticipation (13,14). Ventral striatal activity is also associated with impulsivity, a hallmark of ADHD (12,13). Recently, the NOS1 gene was identified as a candidate gene for ADHD and other impulsivity disorders (15). A variant in this gene was also among the top findings of a genome-wide association study in ADHD (3). NOS1 encodes nitric oxide synthase 1. Nitric oxide, the product of this enzyme's activity, acts as the second messenger downstream of the N-methyl-d-aspartate receptor and interacts with both the dopaminergic and serotonergic systems in the human brain. Nitric oxide inhibits monoamine transporters, thereby modulating the dopamine and noradrenalin concentration in the extracellular space (16). In addi-(A m J P sy c h ia try 2 0 1 1 ; 1 6 8 :1 0 9 9 -1 1 0 6 ) N itric O x id e S y n th a se G e n o ty p e M o d u la tio n o f Im p u lsiv ity a n d Ve n tra l S tria ta l A c tiv ity in A d u lt A D H D P a tie n ts a n d H e a lth y C o m p a riso n S u b je c ts O b je c tiv e : Attention deficit hyperactivity disorder (AD HD ) is a highly heritable disorder. The NO S1 gene encoding nitric oxide synthase is a candidate gene for AD HD and has been previously linked w ith im pulsivity. In the present study, the authors investigated the effect of a functional variable num ber of tandem repeats (VNTR ) polym orphism in NO S1 (NO S1 exon 1f-VNTR ) on the processing of rew ards, one of the cognitive deficits in AD HD. M e th o d :A sam ple of 136 participants, consisting of 87 adult AD HD patients and 49 healthy com parison subjects, completed a rew ard-related im pulsivity task. A total of 104 participants also underw ent functional m agnetic resonance im aging during a rew ard anticipation task. The effect of the NO S1 exon 1f-VNTR genotype on rew ard-related im pulsivity and rew ard-related ventral striatal activity w as exam ined.R e s u lts : AD HD patients had higher impulsivity scores and low er ventral striatal activity than healthy com parison subjects. The association betw een the short allele and increased im pulsivity w as confirm ed. How ever, independent of disease status, hom ozygous carriers of the short allele of NO S1, the AD HD risk genotype, dem onstrated higher ventral striatal activity than carriers of the other NO S1 VNTR genotypes.C o n c lu s io n s : The authors suggest that the NO S1 genotype influences im pulsivity and its relation w ith AD HD is m ediated through effects on this behavioral tr...

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“…97 DETANONOate promotes neuronal differentiation and neurite outgrowth in both young and older SVZ neurospheres. 104 DETA-NONOate modulation of SVZ cell differentiation is controlled by N-cadherin, ␤-catenin, and neurogenin 1 gene expression. 104 The NO-cGMP-protein kinase G (PKG) signaling pathway facilitates communication between neurons and glia, 105 and enhances neurotrophin-induced neurite outgrowth.…”

Section: Pde-5 Inhibitors Cgmp and No Donorsmentioning

confidence: 99%

“…104 DETA-NONOate modulation of SVZ cell differentiation is controlled by N-cadherin, ␤-catenin, and neurogenin 1 gene expression. 104 The NO-cGMP-protein kinase G (PKG) signaling pathway facilitates communication between neurons and glia, 105 and enhances neurotrophin-induced neurite outgrowth. 106 As described above, EPO and EPOR promote adult neurogenesis and migration of regenerating neurons during postinjury recovery.…”

Section: Pde-5 Inhibitors Cgmp and No Donorsmentioning

confidence: 99%

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Chen

Chopp

2006

NeuroRX

153

114

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Summary:There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrowderived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.

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N-cadherin mediates nitric oxide-induced neurogenesis in young and retired breeder neurospheres

Cited by 40 publications

References 43 publications

Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation

Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation

Nitric Oxide Synthase Genotype Modulation of Impulsivity and Ventral Striatal Activity in Adult ADHD Patients and Healthy Comparison Subjects

Neurorestorative treatment of stroke: Cell and pharmacological approaches

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