Chain Migration of Neuronal Precursors

Lois, Carlos; García‐Verdugo, José Manuel; Alvarez-Buylla, Arturo

doi:10.1126/science.271.5251.978

Cited by 1,208 publications

(1,016 citation statements)

References 47 publications

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“…In vivo, following Y27632 infusion into the lateral ventricle, the ensuing decrease in NPC-NPC association appeared to negatively impact on the basic navigational capability of the NPCs to the OB, resulting in a partial loss of directed migration. Physiologically, NPCs in the SVZ/RMS migrate in a closely associated chain formation, ensheathed by networks of glial fibers [7,9,10,53]. Close association among NPCs or between NPCs and glial cells within the RMS is believed to be important to maintain chain migration, as disruption to the cell-cell interactions disrupts NPC chain migration.…”

Section: Regulation Of Npc Morphology and Migration By Rho Gtpase Sigmentioning

confidence: 99%

“…For NPCs, molecules such as integrins [3,4] and cell adhesion molecules, such as the NPC marker, polysialated neural cell adhesion molecule (PSA-NCAM) [5][6][7][8][9][10][11], are involved in providing the framework for migration, whereas a number of growth factors, such as epidermal growth factor (EGF) confer the capacity for migration [12,13]. These factors make the cells competent to migrate and may be permissive factors allowing NPCs to respond to directional cues.…”

Section: Introductionmentioning

confidence: 99%

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The Rho Kinase Pathway Regulates Mouse Adult Neural Precursor Cell Migration

et al. 2011

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Adult neural precursor cells (NPCs) in the subventricular zone (SVZ) normally migrate via the rostral migratory stream (RMS) to the olfactory bulb (OB). Following neural injury, they also migrate to the site of damage. This study investigated the role of Rho-dependent kinase (ROCK) on the migration of NPCs in vitro and in vivo. In vitro, using neurospheres or SVZ explants, inhibition of ROCK using Y27632 promoted cell body elongation, process protrusion, and migration, while inhibiting NPC chain formation. It had no effect on proliferation, apoptosis, or differentiation. Both isoforms of ROCK were involved. Using siRNA, knockdown of both ROCK1 and ROCK2 was required to promote NPC migration and morphological changes; knockdown of ROCK2 alone was partially effective, with little/no effect of knockdown of ROCK1 alone. In vivo, infusion of Y27632 plus Bromodeoxyuridine (BrdU) into the lateral ventricle for 1 week reduced the number of BrdU-labeled NPCs in the OB compared with BrdU infusion alone. However, ROCK inhibition did not affect the tangential-to-radial switch of NPC migration, as labeled cells were present in all OB layers. The decrease in NPC number at the OB was not attributed to a decrease in NPCs at the SVZ. However, ROCK inhibition decreased the density of BrdU-labeled cells in the RMS and increased the distribution of these cells to ectopic brain regions, such as the accessory olfactory nucleus, where the majority differentiated into neurons. These findings suggest that ROCK signaling regulates NPC migration via regulation of cell-cell contact and chain migration.

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Section: Regulation Of Npc Morphology and Migration By Rho Gtpase Sigmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Rho Kinase Pathway Regulates Mouse Adult Neural Precursor Cell Migration

et al. 2011

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“…In mammals, neural stem cells of the subventricular zone (SVZ) continually generate transit-amplifying glial and neuronal daughters, at least some of which give rise to new neurons [67][68][69][70]; the latter are typically recruited anteriorly to the olfactory bulb as GABAergic interneurons of several phenotypes [68,[71][72][73][74][75]. Olfactory neuronal recruitment is rapid; in mice, it takes approximately 15 days for neuronally restricted progenitor cells of the SVZ to migrate through the rostral migratory stream to the olfactory bulb, traversing a distance of 3 to 5 mm, wherein they differentiate into olfactory interneurons [67,76,77] (for more detail see Whitman and Greer [78] and Abrous et al [79]).…”

Section: Induced Neurogenesis From Endogenous Neural Stem Cells As a mentioning

confidence: 99%

Cellular Therapy and Induced Neuronal Replacement for Huntington's Disease

Benraiss

Goldman

2011

Neurotherapeutics

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“…There are several niches in the adult brain in which NSCs persist throughout life and can respond to injurious processes [15][16][17][18]. New neurons are continuously generated in the anterior subventricular zone (SVZ) of adult rodents, from which they migrate via the rostral migratory stream to the olfactory bulb [19][20][21][22][23], and in the subgranular zone of the hippocampal dentate gyrus of both adult rodents [24][25][26][27] and humans [6,28]. The subependymal cell layer of the ventricles [29] and spinal cord [30] contains stem cells that give rise to both neurons and glia.…”

Section: Glial Progenitor Cells In the Adult Central Nervous Systemmentioning

confidence: 99%

Cell Therapy for Multiple Sclerosis

Ben‐Hur

2011

Neurotherapeutics

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The spontaneous recovery observed in the early stages of multiple sclerosis (MS) is substituted with a later progressive course and failure of endogenous processes of repair and remyelination. Although this is the basic rationale for cell therapy, it is not clear yet to what degree the MS brain is amenable for repair and whether cell therapy has an advantage in comparison to other strategies to enhance endogenous remyelination. Central to the promise of stem cell therapy is the therapeutic plasticity, by which neural precursors can replace damaged oligodendrocytes and myelin, and also effectively attenuate the autoimmune process in a local, nonsystemic manner to protect brain cells from further injury, as well as facilitate the intrinsic capacity of the brain for recovery. These fundamental immunomodulatory and neurotrophic properties are shared by stem cells of different sources. By using different routes of delivery, cells may target both affected white matter tracts and the perivascular niche where the trafficking of immune cells occur. It is unclear yet whether the therapeutic properties of transplanted cells are maintained with the duration of time. The application of neural stem cell therapy (derived from fetal brain or from human embryonic stem cells) will be realized once their purification, mass generation, and safety are guaranteed. However, previous clinical experience with bone marrow stromal (mesenchymal) stem cells and the relative easy expansion of autologous cells have opened the way to their experimental application in MS. An initial clinical trial has established the probable safety of their intravenous and intrathecal delivery. Short-term follow-up observed immunomodulatory effects and clinical benefit justifying further clinical trials.

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Chain Migration of Neuronal Precursors

Cited by 1,208 publications

References 47 publications

The Rho Kinase Pathway Regulates Mouse Adult Neural Precursor Cell Migration

The Rho Kinase Pathway Regulates Mouse Adult Neural Precursor Cell Migration

Cellular Therapy and Induced Neuronal Replacement for Huntington's Disease

Cell Therapy for Multiple Sclerosis

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