Transforming growth factor alpha acts as a gliatrophin for mouse and human astrocytes

Sharif, Ariane; Prévot, Vincent; Raffi, François; Allet, Cécile; Studler, J.-M.; Canton, B.; Chneiweiss, Hervé; Junier, Marie Pierre

doi:10.1038/sj.onc.1209443

Cited by 27 publications

(34 citation statements)

References 69 publications

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“…TGFa overexpression is found in about 80% of them, and is observed from the initial steps of their development (Junier, 2000), whereas the overexpression of erbB1 appears in 20-40% of them in later phases (Wechsler-Reya and Scott, 2001). We previously showed that TGFa acts as a gliatrophin on mouse and human cortical astrocytes, promoting their growth as well as their survival (Sharif et al, 2006b), in agreement with the recent report of increased astrocyte apoptosis in erbB1 knockout mice (Wagner et al, 2006). These results suggest that TGFa might participate in the early stages of tumoral transformation through the deregulation of astrocyte proliferation and apoptosis.…”

Section: Introductionsupporting

confidence: 90%

“…TGFa effect was fully reversed upon serum addition (not shown). To check for the specificity of TGFa effect, we evaluated the activation state of erbB1 that we previously evidenced to be activated up to 3 days of TGFa treatment (Sharif et al, 2006b). We observed that the activated, phosphorylated form of erbB1 was still detected after 7 DIV in the presence of TGFa, despite downregulation of the protein levels of the receptor (Supplementary Figure 1).…”

Section: Resultsmentioning

confidence: 95%

“…Interestingly, we and others noted that several days of TGFa exposure leads in vitro to morphological alterations of wild-type astrocytes, reminiscent of the bipolar shape of a population of neural progenitors, the radial glial cells (Miller et al, 1996;Zhou et al, 2001;Figiel et al, 2003;Liu and Neufeld, 2004;Sharif et al, 2006b). …”

Section: Introductionmentioning

confidence: 90%

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Transforming growth factor α promotes sequential conversion of mature astrocytes into neural progenitors and stem cells

et al. 2006

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Section: Introductionsupporting

confidence: 90%

Section: Resultsmentioning

confidence: 95%

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Transforming growth factor α promotes sequential conversion of mature astrocytes into neural progenitors and stem cells

et al. 2006

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“…Several EGFR ligands have been identified including EGF, HB-EGF, and TGF-␣ (Kornblum et al, 1999;Sharif et al, 2006). Using specific neutralizing antibodies, we next attempted to identify which of these ligands may be involved in TWEAK-mediated astrocyte proliferation.…”

Section: Tweak and Fn14 Expression In Cns-derived Cellsmentioning

confidence: 99%

Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Induces Astrocyte Proliferation through the Activation of Transforming-Growth Factor-α/Epidermal Growth Factor Receptor Signaling Pathway

Rousselet¹,

Traver

Monnet

et al. 2012

Mol Pharmacol

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Reactive astrogliosis is beneficial in many aspects; however, it is also detrimental in some pathological states such as the development of lethal brain tumors. It is therefore crucial to understand the mechanisms regulating astrocyte proliferation. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor family, was shown to stimulate astrocyte proliferation in vitro. Herein, we further characterize the mitogenic potential of TWEAK on central nervous system cells. Among these cells, astrocytes express the highest level of TWEAK and Fn14 transcripts, suggesting that they are particularly sensitive to TWEAK stimulation. Using in vitro model systems, we found that TWEAK was as potent as epidermal growth factor (EGF) (a prototypical astrocyte mitogen) in mediating astrocyte proliferation.However, its mitogenic activity was delayed compared with that of EGF, suggesting distinct mechanisms of action. Using cell signaling pathway inhibitors, neutralizing antibodies, and protein assays, we further show that the mitogenic activity of TWEAK on primary astrocytes requires stimulation of the transforming growth factor-␣ (TGF-␣) and of the epidermal growth factor receptor (EGFR) signaling pathway through extracellular signal-regulated kinase and p38 mitogen-activated protein kinase activation. In aggregates, our data demonstrate that TWEAK acts as a potent astrocyte mitogen through the induction of a TGF-␣/EGFR signaling pathway. We anticipate that description of such a mechanism may allow novel approaches to human pathologies associated with astrocyte proliferation.

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“…Transforming growth factor ␣ (TGF␣) is a critical regulator of astrocyte formation, and TGF␣ signaling is frequently deregulated in gliomas (Sibilia et al 1998;Junier 2000;Wechsler-Reya and Scott 2001). Prolonged exposure to TGF␣, which is overexpressed in earlier stages of glioma, can cause astrocytes in vitro to regress into neural progenitor-like cells (Sharif et al 2006(Sharif et al , 2007.…”

Section: Potential Mechanisms Involved In Erbb2 Reinduced Astrocytesmentioning

confidence: 99%

Reinduction of ErbB2 in astrocytes promotes radial glial progenitor identity in adult cerebral cortex

Ghashghaei¹,

Weimer²,

Schmid

et al. 2007

Genes Dev.

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Radial glial cells play a critical role in the construction of mammalian brain by functioning as a source of new neurons and by providing a scaffold for radial migration of new neurons to their target locations. Radial glia transform into astrocytes at the end of embryonic development. Strategies to promote functional recovery in the injured adult brain depend on the generation of new neurons and the appropriate guidance of these neurons to where they are needed, two critical functions of radial glia. Thus, the competence to regain radial glial identity in the adult brain is of significance for the ability to promote functional repair via neurogenesis and targeted neuronal migration in the mature brain. Here we show that the in vivo induction of the tyrosine kinase receptor, ErbB2, in mature astrocytes enables a subset of them to regain radial glial identity in the mature cerebral cortex. These new radial glial progenitors are capable of giving rise to new neurons and can support neuronal migration. These studies indicate that ErbB2 signaling critically modulates the functional state of radial glia, and induction of ErbB2 in distinct adult astrocytes can promote radial glial identity in the mature cerebral cortex.[Keywords: Cortical development; neurogenesis; radial glia; ErbB receptors; neuregulins] Supplemental material is available at http://www.genesdev.org.

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Transforming growth factor alpha acts as a gliatrophin for mouse and human astrocytes

Cited by 27 publications

References 69 publications

Transforming growth factor α promotes sequential conversion of mature astrocytes into neural progenitors and stem cells

Transforming growth factor α promotes sequential conversion of mature astrocytes into neural progenitors and stem cells

Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Induces Astrocyte Proliferation through the Activation of Transforming-Growth Factor-α/Epidermal Growth Factor Receptor Signaling Pathway

Reinduction of ErbB2 in astrocytes promotes radial glial progenitor identity in adult cerebral cortex

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