Early acquisition of typical metabolic features upon differentiation of mouse neural stem cells into astrocytes

Jf, Brunet; Grollimund, L; Chatton, Jean–Yves; Lengacher, Sylvain; Magistretti, Pierre J.; Villemure, J.-G.; Pellerin, Luc

doi:10.1002/glia.10348

Cited by 49 publications

(53 citation statements)

References 38 publications

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“…Fetal calf serum was found to induce the expression of glutamine synthetase (Loo et al, 1995), an enzyme typically associated with mature astrocytes as it participates to glutamate recycling, which is a major astrocytic function (Ereciñ ska and Silver, 1990). Our previous data also showed dramatic effects of FCS on a number of specific astroglial proteins and/or mRNAs such as GFAP, vimentin, or S100b, and on expression of key metabolic proteins such as the glutamate aspartate transporter (GLAST), the monocarboxylate transporter 1 (MCT1), and the a 2 -subunit of the Na + /K + ATPase (Brunet et al, 2004). Moreover, metabolic features of mature astrocytes such as glutamate uptake or glutamate-induced activation of glycolysis emerged after treatment with FCS.…”

Section: Discussionmentioning

confidence: 84%

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Glycogen Metabolism as a Marker of Astrocyte Differentiation

Brunet¹,

Allaman²,

Magistretti³

et al. 2009

J Cereb Blood Flow Metab

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Glycogen is a hallmark of mature astrocytes, but its emergence during astrocytic differentiation is unclear. Differentiation of E14 mouse neurospheres into astrocytes was induced with fetal bovine serum (FBS), Leukemia Inhibitory Factor (LIF), or Ciliary Neurotrophic Factor (CNTF). Cytochemical and enzymatic analyses showed that glycogen is present in FBS-or LIF-but not in CNTF-differentiated astrocytes. Glycogenolysis was induced in FBS-and LIF-differentiated astrocytes but glycogen resynthesis was observed only with FBS. Protein targeting to glycogen mRNA expression appeared with glial fibrillary acidic protein and S100b in FBS and LIF conditions but not with CNTF. These results show that glycogen metabolism constitutes a useful marker of astrocyte differentiation.

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Section: Discussionmentioning

confidence: 84%

“…Neurospheres were prepared essentially as described previously (Brunet et al, 2004). For details, see Supplementary information.…”

Section: Neurosphere Culturesmentioning

confidence: 99%

Glycogen Metabolism as a Marker of Astrocyte Differentiation

Brunet¹,

Allaman²,

Magistretti³

et al. 2009

J Cereb Blood Flow Metab

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“…It is likely that these two proteins contribute to the astrocytic lineage selection of NSPCs observed in this study, since both CNTF and LIF previously have been demonstrated to potently induce astroglial differentiation of NSPCs 173,[188][189][190] .…”

Section: Interactions Between Reactive Astrocytes and Nspcsmentioning

confidence: 78%

“…The expression levels of CNTF and LIF, proteins that previously have been associated with reactive astrocytes 30,186,187 and astrocytic differentiation of NSPCs 173,[188][189][190] , were determined. In these experiments, we found that both CNTF and LIF were up-regulated in CM from lesioned astrocytes.…”

Section: Lif and Cntf Are Released By Reactive Astrocytes In Vitro [I]mentioning

confidence: 99%

Efficient non-viral transfection of adult neural stem/progenitor cells, without affecting viability, proliferation or differentiation

2005

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Stroke is one of the leading causes of chronic disability and death in the Western world. Today, no treatment can repair the cellular loss associated with an ischemic lesion. However, the discovery and dynamic regulation of neural stem/progenitor cells in the adult mammalian brain has resulted in exciting possibilities for future therapeutic interventions. Endogenous or grafted neural stem/progenitor cells are activated following an ischemic insult. These cells undergo directed migration towards infarcted areas, and differentiate in response to the insult. Unfortunately, the results of this regenerative effort are limited compared to the amount of tissue loss. This could be due to low survival of the recruited cells, but could also be explained by insufficient activation or dysfunctional lineage selection. Whether the lineage selection of neural stem/progenitor cells is altered following a lesion in the brain, what signals that are responsible for their activation or whether these cells can participate in post-lesion regeneration, astrogliosis or neuroprotection have yet to become clear. A greater understanding of these processes is necessary for finding ways to improve the endogenous regenerative capacity. We found that reactive astrocytes, a prominent part of the post-ischemic environment, induced astroglial differentiation of adult neural stem/progenitor cells in vitro. Moreover, astrocytes derived from these cells were shown to participate in glial scar formation in vitro. After studying gene expression in the peri-infarct region following focal ischemia, the expression of several genes was induced. We chose to focus our attention on one of these genes and its product, thyrotropin-releasing hormone (TRH). Immunoreactivity for TRH was found in several areas in both lesioned and intact brain regions, including in microglia present in the areas surrounding the lesion. Furthermore, TRH receptors were expressed on cultured neural stem/progenitor cells and TRH potently induced the proliferation of these cells. TRH is an interesting target for stroke treatment, but it also has many central effects in the brain and systemic administration may prove problematic. An interesting protocol for local delivery of TRH would be by grafting stem/progenitor cells, genetically engineered to secrete the peptide. In order to create a foundation for neuroprotective gene therapy, we developed efficient methods for non-viral transfection of neural stem/progenitor cells. Since neural stem/progenitor cells migrate towards the ischemic area we wanted to investigate whether these cells secreted factors that could protect neurons against excitotoxicity, the main inducer of cell death following a stroke. Mass spectrometric analysis of factors secreted from cultured neural stem/progenitor cells led to the identification of a novel neuroprotective peptide, which we termed pentinin. This peptide potently reduced excitotoxicity in both mature and immature neurons in an ex vivo hippocampal slice model. The results presented in this the...

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“…It was diluted in PBS (−) with DAPI (0.5 µg/ml; Sigma Chemical Co.) to identify the nuclei. Expression of glial fibrillary acidic protein (GFAP) and nestin was analyzed to detect reactive astrocytes (Suzuki et al 2003;Brunet et al 2004). GFAP is a marker of astrocytes.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Maternal Undernutrition with Vaginal Inflammation Impairs the Neonatal Oligodendrogenesis in Mice

Ito

Hoshiai

Tanabe

et al. 2011

Tohoku J. Exp. Med.

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Maternal undernutrition and infection during pregnancy may impair development of oligodendrocytes, thereby increasing risks of neuropsychiatric disorders of their children. We analyzed the effects of those risk factors on oligodendrogenesis in fetal and neonatal brains. Female mice were given low-protein or regular food for 2 weeks before their pregnancy. On the 14th day of pregnancy, they received a transvaginal injection of lipopolysaccharide to induce inflammation or control solution, consisting of four groups, depending on nutritional conditions with or without vaginal inflammation. We collected fetal brains on embryonic day (E) 17 for evaluating oligodendrocyte precursor cells (OPCs) and neonatal brains on postnatal day (P) 7 for evaluating mature oligodendrocytes. OPCs and mature oligodendrocytes were identified as positive immunostaining for oligodendrocyte-lineage transcription factor 2 and myelin basic protein, respectively. There was no difference in the number of OPCs in E17 brains among the four groups, suggesting that nutritional restriction with or without inflammation exerts no noticeable influence on the differentiation of OPCs. However, the number of mature oligodendrocytes was decreased in P7 brains obtained from nutrient-restricted mice with inflammation, suggesting that their combination impairs oligodendrogenesis in the neonatal brain. We also analyzed reactive astrocytes that express both glial fibrillary acidic protein and nestin for evaluating brain inflammation. The population of reactive astrocytes was increased in P7 brains derived from mice with LPS injection, irrespective of nutritional restriction, indicating that maternal vaginal inflammation induces neonatal brain inflammation. The maternal management of both nutrition and infection is crucial to prevent neuropsychiatric disorders of the children.

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Early acquisition of typical metabolic features upon differentiation of mouse neural stem cells into astrocytes

Cited by 49 publications

References 38 publications

Glycogen Metabolism as a Marker of Astrocyte Differentiation

Glycogen Metabolism as a Marker of Astrocyte Differentiation

Efficient non-viral transfection of adult neural stem/progenitor cells, without affecting viability, proliferation or differentiation

Maternal Undernutrition with Vaginal Inflammation Impairs the Neonatal Oligodendrogenesis in Mice

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