Neuropeptide Y Promotes Neurogenesis in Murine Subventricular Zone

Agasse, Fabienne; Bernardino, Liliana; Kristiansen, Heidi; Christiansen, Søren H.; Ferreira, Raquel; Silva, Bruno; Grade, Sofia; Woldbye, David P. D.; Malva, João O.

doi:10.1634/stemcells.2008-0056

Cited by 90 publications

(87 citation statements)

References 51 publications

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“…Also, as reported previously by us, the P-JNK staining co-localized with Tau, a microtubule-associated protein able to modulate the stability of axonal microtubules in mature and immature neurons [29,30].…”

Section: Mir-124 Nps Promote Axonogenesissupporting

confidence: 85%

“…In these conditions, SVZ cells grow in suspension and generate neurospheres that are rich in neural and progenitor stem cells at distinct stages of differentiation and with proliferative and selfrenewing abilities, as previously shown by us [7,24,[27][28][29][30]. Five to six-day-old neurospheres were seeded onto 0.1 mg/mL poly-D-lysine-(PDL; Sigma-Aldrich Co. Zeiss, Jena, Germany).…”

Section: Svz Cell Cultures and Experimental Treatmentsmentioning

confidence: 99%

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MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

143

128

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Modulation of the subventricular zone (SVZ) neurogenic niche can enhance brain repair in several disorders including Parkinson's disease (PD). Herein, we used biocompatible and traceable polymeric nanoparticles (NPs) containing perfluoro-1,5-crown ether (PFCE) and coated with protamine sulfate to complex microRNA-124 (miR-124), a neuronal fate determinant. The ability of NPs to efficiently deliver miR-124 and prompt SVZ neurogenesis and brain repair in PD was evaluated. In vitro, miR-124 NPs were efficiently internalized by neural stem/progenitors cells and neuroblasts and promoted their neuronal commitment and maturation. The expression of Sox9 and Jagged1, two miR-124 targets and stemness-related genes, were also decreased upon miR-124 NP treatment. In vivo, the intracerebral administration of miR-124 NPs increased the number of migrating neuroblasts that reached the granule cell layer of the olfactory bulb, both in healthy and in a 6-hydroxydopamine (6-OHDA) mouse model for PD.MiR-124 NPs were also able to induce migration of neurons into the lesioned striatum of 6-OHDA-treated mice. Most importantly, miR-124 NPs proved to ameliorate motor symptoms of 6-OHDA mice, monitored by the apomorphine-induced rotation test.Altogether, we provide clear evidences to support the use of miR-124 NPs as a new therapeutic approach to boost endogenous brain repair mechanisms in a setting of neurodegeneration.

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Section: Mir-124 Nps Promote Axonogenesissupporting

confidence: 85%

Section: Svz Cell Cultures and Experimental Treatmentsmentioning

confidence: 99%

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

143

128

View full text Add to dashboard Cite

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“…(43) Similarly, NPY has been shown in mice to promote the proliferation of neuronal progenitor cells in the dentate gyrus of the hippocampus (28,44) and also in the subventricular zone. (45,46) Interestingly, in all cases, the Y receptor mediating these effects is the Y1 receptor. Our findings in the study of stem cells in the bone environment further advance these insights to show that Y1 may act as a master switch that may increase bone and fat formation via effects on MSCs.…”

Section: Discussionmentioning

confidence: 99%

Critical role for Y1 receptors in mesenchymal progenitor cell differentiation and osteoblast activity

Lee

Doyle

Sainsbury

et al. 2010

Journal of Bone and Mineral Research

103

135

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The neuropeptide Y (NPY) system has been implicated in the regulation of bone homeostasis and osteoblast activity, but the mechanism behind this is unclear. Here we show that Y1 receptor signaling is directly involved in the differentiation of mesenchymal progenitor cells isolated from bone tissue, as well as the activity of mature osteoblasts. Importantly, the mRNA levels of two key osteogenic transcription factors, runx2 and osterix, as well as the adipogenic transcription factor PPAR-g, were increased in long bones of Y1 À/À mice compared with wild-type mice. In vitro, bone marrow stromal cells (BMSCs) isolated from Y1 À/À mice formed a greater number of mineralized nodules under osteogenic conditions and a greater number of adipocytes under adipogenic conditions than controls. In addition, both the number and size of fibroblast colony-forming units formed in vitro by purified osteoprogenitor cells were increased in the absence of the Y1 receptors, suggestive of enhanced proliferation and osteogenesis. Furthermore, the ability of two specific populations of mesenchymal progenitor cells isolated from bone tissue, an immature mesenchymal stem cell population and a more committed osteoprogenitor cell population, to differentiate into osteoblasts and adipocytes in vitro was enhanced in the absence of Y1 receptor signaling. Finally, Y1 receptor deletion also enhanced the mineral-producing ability of mature osteoblasts, as shown by increased in vitro mineralization by BMSCs isolated from osteoblast-specific Y1 À/À mice. Together these data demonstrate that the NPY system, via the Y1 receptor, directly inhibits the differentiation of mesenchymal progenitor cells as well as the activity of mature osteoblasts, constituting a likely mechanism for the high-bone-mass phenotype evident in Y1 À/À mice. ß

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“…The SVZ was dissected as previously described [16], and the tissue was digested in 0.025% trypsin/0.265 mM EDTA, for 20 minutes at 37 C, and mechanically dissociated. Single cells were resuspended in fresh D-MEM/F-12 with GlutaMAX-I, supplemented with 1% B27, 1% antibiotic (10,000 units/ml of penicillin, 10 mg/ml streptomycin), 10 ng/ml EGF and 10 ng/ml basic fibroblast growth factor (bFGF), and plated on uncoated Petri dishes at a density of 3,000 cells per square centimeter.…”

Section: Subventricular Zone Cell Culturesmentioning

confidence: 99%

Nitric Oxide Stimulates the Proliferation of Neural Stem Cells Bypassing the Epidermal Growth Factor Receptor

et al. 2010

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Nitric oxide (NO) was described to inhibit the proliferation of neural stem cells. Some evidence suggests that NO, under certain conditions, can also promote cell proliferation, although the mechanisms responsible for a potential proliferative effect of NO in neural stem cells have remained unaddressed. In this work, we investigated and characterized the proliferative effect of NO in cell cultures obtained from the mouse subventricular zone. We found that the NO donor NOC-18 (10 lM) increased cell proliferation, whereas higher concentrations (100 lM) inhibited cell proliferation. Increased cell proliferation was detected rapidly following exposure to NO and was prevented by blocking the mitogen-activated kinase (MAPK) pathway, independently of the epidermal growth factor (EGF) receptor. Downstream of the EGF receptor, NO activated p21Ras and the MAPK pathway, resulting in a decrease in the nuclear presence of the cyclin-dependent kinase inhibitor 1, p27 KIP1 , allowing for cell cycle progression. Furthermore, in a mouse model that shows increased proliferation of neural stem cells in the hippocampus following seizure injury, we observed that the absence of inducible nitric oxide synthase (iNOS 2/2 mice) prevented the increase in cell proliferation observed following seizures in wild-type mice, showing that NO from iNOS origin is important for increased cell proliferation following a brain insult. Overall, we show that NO is able to stimulate the proliferation of neural stem cells bypassing the EGF receptor and promoting cell division. Moreover, under pathophysiological conditions in vivo, NO from iNOS origin also promotes proliferation in the hippocampus. STEM CELLS

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Neuropeptide Y Promotes Neurogenesis in Murine Subventricular Zone

Abstract: ABSTRACT

Cited by 90 publications

References 51 publications

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Critical role for Y1 receptors in mesenchymal progenitor cell differentiation and osteoblast activity

Nitric Oxide Stimulates the Proliferation of Neural Stem Cells Bypassing the Epidermal Growth Factor Receptor

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