Identity crisis for adult periventricular neural stem cells: subventricular zone astrocytes, ependymal cells or both?

Chojnacki, Andrew; Mak, Gloria; Weiss, Samuel

doi:10.1038/nrn2571

Cited by 172 publications

(149 citation statements)

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“…2008; Chojnacki et al. 2009) migrating through a channel of interwoven astrocytes, the rostral migratory stream (RMS), to the olfactory bulb. The SVZ niche is separated from the cerebrospinal fluid (CSF) of the ventricles via a thin layer of multiciliated ependymal cells.…”

Section: Introductionmentioning

confidence: 99%

Depletion of neural stem cells from the subventricular zone of adult mouse brain using cytosine b‐Arabinofuranoside

et al. 2015

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IntroductionNeural stem cells (NSCs) reside along the ventricular axis of the mammalian brain. They divide infrequently to maintain themselves and the down‐stream progenitors. Due to the quiescent property of NSCs, attempts to deplete these cells using antimitotic agents such as cytosine b‐Aarabinofuranoside (Ara‐C) have not been successful. We hypothesized that implementing infusion gaps in Ara‐C kill paradigms would recruit the quiescent NSCs and subsequently eliminate them from their niches in the subventricular zone (SVZ).MethodsWe infused the right lateral ventricle of adult mice brain with 2% Ara‐C using four different paradigms—1: one week; 2: two weeks; 3, 4: two weeks with an infusion gap of 6 and 12 h on day 7. Neurosphere assay (NSA), neural colony‐forming cell assay (N‐CFCA) and immunofluorescent staining were used to assess depletion of NSCs from the SVZ.ResultsNeurosphere formation dramatically decreased in all paradigms immediately after Ara‐C infusion. Reduction in neurosphere formation was more pronounced in the 3rd and 4th paradigms. Interestingly 1 week after Ara‐C infusion, neurosphere formation recovered toward control values implying the presence of NSCs in the harvested SVZ tissue. Unexpectedly, N‐CFCA in the 3rd paradigm, as one of the most effective paradigms, did not result in formation of NSC‐derived colonies (colonies >2 mm) even from SVZs harvested 1 week after completion of Ara‐C infusion. However, formation of big colonies with serial passaging capability, again confirmed the presence of NSCs.ConclusionsOverall, these data suggest Ara‐C kill paradigms with infusion gaps deplete NSCs in the SVZ more efficiently but the niches would repopulate even after the most vigorous kill paradigm used in this study.

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Section: Introductionmentioning

confidence: 99%

Depletion of neural stem cells from the subventricular zone of adult mouse brain using cytosine b‐Arabinofuranoside

et al. 2015

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“…However, GFAP is expressed in some nerve cell populations, including hippocampal neurons of older individuals (1). It is also expressed in some precursor populations of nerve cells as well as in cells that can give rise to both nerve and glia (2)(3)(4). Finally, the expression levels of GFAP within individual cells is extremely variable, and higher expression levels may limit the tumorigenicity of subpopulations of cells within glioblastomas (5,6).…”

Section: The Intermediate Filament Protein Glial Fibrillary Acidic Prmentioning

confidence: 99%

Synergistic Effect of Retinoic Acid and Cytokines on the Regulation of Glial Fibrillary Acidic Protein Expression

Herrera

Chen

Schubert

2010

Journal of Biological Chemistry

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Glial fibrillary acidic protein (GFAP) is the main astroglial marker during astrogliogenesis, but it is also expressed in other cell types, including neural stem cells and old neurons. Activation of the JAK/STAT pathway by the IL-6 family of cytokines is the canonical pathway regulating GFAP expression, whereas retinoic acid is thought to be the only inducer of GFAP to operate independently of this pathway. Here, we show that retinoic acid receptor ␣ not only links retinoic acid signaling to the canonical cytokine-stimulated pathway leading to GFAP expression but that it also plays a key role in the synergistic actions of retinoic acid and cytokines on this pathway. Cytokines both potentiate retinoic acid receptor ␣ expression and enhance its binding to DNA and to the Stat3-p300/CBP-Smad transcriptional complex, the cornerstone of the canonical pathway. PI3K is upstream to all the key events leading to the expression of GFAP. Our results give new insights about the role of retinoic acid signaling in GFAP expression.The intermediate filament protein glial fibrillary acidic protein (GFAP) 2 is considered a cell type-specific marker for astrocytes. However, GFAP is expressed in some nerve cell populations, including hippocampal neurons of older individuals (1). It is also expressed in some precursor populations of nerve cells as well as in cells that can give rise to both nerve and glia (2-4). Finally, the expression levels of GFAP within individual cells is extremely variable, and higher expression levels may limit the tumorigenicity of subpopulations of cells within glioblastomas (5, 6). Because of the wide range of cellular phenotypes associated with GFAP, it is important to understand the molecular mechanisms that regulate its expression.The GFAP is regulated in part by the secretion of factors into the extracellular space (7). The canonical pathway for GFAP expression in astrocytes is triggered by the binding of cytokines from the interleukin-6 (IL-6) family to their receptors. These receptors subsequently activate the JAK/STAT intracellular pathway, leading to the expression of GFAP in astrocytes (7-9). Most of the other pathways known to participate in GFAP expression are connected at some point to this canonical pathway (10, 11). For example, some members of the tumor growth factor-␤ (TGF-␤) superfamily of cytokines have little or no effect on GFAP synthesis by themselves, but they strongly potentiate GFAP induced by the IL-6 family of cytokines. They do so by triggering the phosphorylation, activation, and heterodimerization of Smad proteins, which then form a more potent transcriptional complex with p300/CBP and Stat3. As a consequence, the expression of GFAP is greatly enhanced (9, 12-14).All-trans-retinoic acid (RA), generally considered to be a neurogenic agent, is in fact a potent inducer of GFAP (14 -18). Studies with pharmacological agonists for the different retinoic acid receptors indicate that retinoic acid-induced GFAP expression is mediated by the activation of retinoic acid receptor (RAR) ␣ ...

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“…Without a doubt, the features shared by the many cellular types of the SVZ contributed to the debate about the true identity of NSCs (for review, Chojnacki et al, 2009). Mitotic cells (astrocytes or B cells) have been generally considered to be the true NSCs, owing to their self-renew capacity and their ability to indefinitely produce neuronal and glial progeny (García-Verdugo et al, 1998;Doetsch et al, 1999).…”

Section: The Svz and Rostral Migratory Stream (Rms): A General Viewmentioning

confidence: 99%

“…Most studies have not observed substantial changes in infarct size after NSCs transplantation (Kelly et al, 2004;Pollock et al, 2006); however, neuroprotective (Lee et al, 2007;Ourednik et al, 2002) and immunomodulatory (Fujiwara et al, 2004;Pluchino et al, 2005) effects of NSCs in addition to their potential for at least some cell replacement (Sinden et al, 1997), have collectively yielded beneficial effects in multiple animal models of neurodegeneration and brain injury, including stroke (Chu et al, 2004;Pollock et al, 2006;Sinden et al, 1997).…”

Section: From Theory To Practice: Nscs Transplant In Rodent Models Ofmentioning

confidence: 99%

Neural Stem Cells: Exogenous and Endogenous Promising Therapies for Stroke

Guerra-Crespo¹,

Herrán-Arita²,

Boronat-García³

et al. 2012

Neural Stem Cells and Therapy

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Identity crisis for adult periventricular neural stem cells: subventricular zone astrocytes, ependymal cells or both?

Cited by 172 publications

References 151 publications

Depletion of neural stem cells from the subventricular zone of adult mouse brain using cytosine b‐Arabinofuranoside

Depletion of neural stem cells from the subventricular zone of adult mouse brain using cytosine b‐Arabinofuranoside

Synergistic Effect of Retinoic Acid and Cytokines on the Regulation of Glial Fibrillary Acidic Protein Expression

Neural Stem Cells: Exogenous and Endogenous Promising Therapies for Stroke

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