Nestin-containing cells express glial fibrillary acidic protein in the proliferative regions of central nervous system of postnatal developing and adult mice

Li, Wei; Shi, Minmin; Chen, L.-W; Cao, Rong; Zhang, P; Chan, Ying-Shing

doi:10.1016/s0165-3806(02)00509-6

Cited by 129 publications

(104 citation statements)

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“…4 D). Coexpression of GFAP and nestin has been observed in cells with morphologic and physiologic properties of astrocytes (Schmidt-Kastner and Humpel, 2002;Wei et al, 2002), raising the possibility of a similar occurrence in our cultures. In support of the interpretation that the GFAPϩ and GFAPϩ/nestinϩ cells infected with the Azip-ATF5 construct were likely to be differentiated astrocytes, essentially none of such cells incorporated BrdU (Fig.…”

Section: Atf5 Represses and Azip-atf5 Leads To Astrocytic Differentmentioning

confidence: 59%

“…3E). We also assessed the expression of nestin, which is present in proliferating embryonic VZ neural progenitors (Eliasson et al, 1999;Wei et al, 2002;Filippov et al, 2003) but also in some astrocytes, especially those in a reactive state (Schmidt-Kastner and Humpel, 2002;Wei et al, 2002). Constitutive ATF5 expression increased the proportion of nestinϩ cells in the cultures by more than threefold (to 60 -80%) (Angelastro et al, 2003), but very few of these coexpressed GFAP (Fig.…”

Section: Overexpression Of Atf5 Induces Progenitor Cells To Remain Inmentioning

confidence: 99%

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Downregulation of Activating Transcription Factor 5 Is Required for Differentiation of Neural Progenitor Cells into Astrocytes

Angelastro¹,

Mason²,

Игнатова³

et al. 2005

J. Neurosci.

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The mechanisms that regulate neural progenitor cell differentiation are primarily unknown. The transcription factor activating transcription factor 5 (ATF5) is expressed in neural progenitors of developing brain but is absent from mature astrocytes and neurons. Here, we demonstrate that ATF5 regulates the conversion of ventricular zone (VZ) and subventricular zone (SVZ) neural progenitors into astrocytes. Constitutive ATF5 expression maintains neural progenitor cell proliferation and blocks their in vitro and in vivo differentiation into astrocytes. Conversely, loss of ATF5 function promotes cell-cycle exit and allows astrocytic differentiation in vitro and in vivo. CNTF, a promoter of astrocytic differentiation, downregulates endogenous ATF5, whereas constitutively expressed ATF5 suppresses CNTF-promoted astrocyte genesis. Unexpectedly, constitutive ATF5 expression in neonatal SVZ cells both in vitro and in vivo causes them to acquire properties and anatomic distributions of VZ cells. These findings identify ATF5 as a key regulator of astrocyte formation and potentially of the VZ to SVZ transition.

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Section: Atf5 Represses and Azip-atf5 Leads To Astrocytic Differentmentioning

confidence: 59%

Section: Overexpression Of Atf5 Induces Progenitor Cells To Remain Inmentioning

confidence: 99%

Downregulation of Activating Transcription Factor 5 Is Required for Differentiation of Neural Progenitor Cells into Astrocytes

Angelastro¹,

Mason²,

Игнатова³

et al. 2005

J. Neurosci.

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“…By 12 DIV, GFAP-expressing cells greatly increased, and accounted for 22 ± 1% of total cells (n = 34 cultures). This increase parallels astrocyte development in vivo (Catalani et al, 2002;Wei et al, 2002;Raponi et al, 2007).…”

Section: Spontaneous Neuronal Impulse Activity Regulates Glial Differmentioning

confidence: 62%

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Cohen

Fields

2008

Neuron Glia Biol.

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Activity-dependent signaling between neurons and astrocytes contributes to experience-dependent plasticity and development of the nervous system. However, mechanisms responsible for neuronglial interactions and the releasable factors that underlie these processes are not well understood. The pro-inflammatory cytokine, leukemia-inhibitory factor (LIF), is transiently expressed postnatally by glial cells in the hippocampus and rapidly up-regulated by enhanced neural activity following seizures. To test the hypothesis that spontaneous neural activity regulates glial development in hippocampus via LIF signaling, we blocked spontaneous activity with the sodium channel blocker tetrodotoxin (TTX) in mixed hippocampal cell cultures in combination with blockers of LIF and purinergic signaling. TTX decreased the number of GFAP-expressing astrocytes in hippocampal cell culture. Furthermore, blocking purinergic signaling by P2Y receptors contributed to reduced numbers of astrocytes. Blocking activity or purinergic signaling in the presence of function-blocking antibodies to LIF did not further decrease the number of astrocytes. Moreover, hippocampal cell cultures prepared from LIF −/− mice had reduced numbers of astrocytes and activity-dependent neuron-glial signaling promoting differentiation of astrocytes was absent. The results show that endogenous LIF is required for normal development of hippocampal astrocytes, and this process is regulated by spontaneous neural impulse activity through the release of ATP.

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“…Nestin may play an important role in remodeling and repairing the postnatal and adult central nervous system. Nestin has also been implicated in myogenesis (Wei et al, 2002).…”

Section: Differential Gene Expression In Mll Knockout Cellsmentioning

confidence: 99%

MLL-mediated transcriptional gene regulation investigated by gene expression profiling

et al. 2003

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Nestin-containing cells express glial fibrillary acidic protein in the proliferative regions of central nervous system of postnatal developing and adult mice

Cited by 129 publications

References 50 publications

Downregulation of Activating Transcription Factor 5 Is Required for Differentiation of Neural Progenitor Cells into Astrocytes

Downregulation of Activating Transcription Factor 5 Is Required for Differentiation of Neural Progenitor Cells into Astrocytes

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

MLL-mediated transcriptional gene regulation investigated by gene expression profiling

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