Conditional deletion of Stat3 promotes neurogenesis and inhibits astrogliogenesis in neural stem cells

Cao, Fang; Hata, Ryuji; Zhu, Pengxiang; Nakashiro, Koh‐ichi; Sakanaka, Masahiro

doi:10.1016/j.bbrc.2010.03.092

Cited by 73 publications

(59 citation statements)

References 27 publications

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“…Third, the levels of whole blood GDNF in patients with mood disorders are significantly lower than those in healthy control subjects [22]. Fourth, STAT3 might mediate astrogliogenesis from neural precursor cell [23,24,25,26,27] and GDNF-dependent mechanisms might exist for activation of STAT3 [28,29]. Our data show that GDNF increases ADP differentiation into astrocytes, but has no effect on ADP proliferation or apoptosis and that STAT3 is required for the effect of GDNF on ADP differentiation into astrocytes.…”

Section: Introductionmentioning

confidence: 72%

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GDNF facilitates differentiation of the adult dentate gyrus-derived neural precursor cells into astrocytes via STAT3

Boku

Nakagawa

Takamura

et al. 2013

Biochemical and Biophysical Research Communications

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While the pro-neurogenic actions of antidepressants in the adult hippocampal dentate gyrus (DG) are thought to be one of the mechanisms through which antidepressants exert their therapeutic actions, antidepressants do not increase proliferation of neural precursor cells derived from the adult DG. Because previous studies showed that antidepressants increase the expression and secretion of glial cell line-derived neurotrophic factor (GDNF) in C6 glioma cells derived from rat astrocytes and GDNF increases neurogenesis in adult DG in vivo, we investigated the effects of GDNF on the proliferation, differentiation and apoptosis of cultured neural precursor cells derived from the adult DG. Data showed that GDNF facilitated the differentiation of neural precursor cells into astrocytes but had no effect on their proliferation or apoptosis. Moreover, GDNF increased the phosphorylation of STAT3, and both a specific inhibitor of STAT3 and lentiviral shRNA for STAT3 decreased their differentiation into astrocytes. Taken together, our findings suggest that GDNF facilitates astrogliogenesis from neural precursor cells in adult DG through activating STAT3 and that this action might indirectly affect neurogenesis.

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Section: Introductionmentioning

confidence: 72%

“…promotes differentiation of neural precursors into astrocytes [24,25,26,27]. On the other hand, it was not known whether GDNF promotes differentiation of neural precursors into astrocytes through STAT3.…”

Section: Discussionmentioning

confidence: 99%

GDNF facilitates differentiation of the adult dentate gyrus-derived neural precursor cells into astrocytes via STAT3

Boku

Nakagawa

Takamura

et al. 2013

Biochemical and Biophysical Research Communications

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“…OALib Journal sis while blocking astrogliogenesis [25]. Inhibitory proteins of JAK-STAT pathway such as SOCS 2, 3 and 6 negatively regulate neuronal differentiation and neurite outgrowth after induction of insulin-like growth factor-1 (IGF-1) and growth hormone [48].…”

Section: /15mentioning

confidence: 99%

“…The discovery of this pathway, especially in the field of cell biology, gives an explanation to the mechanism of gene regulation that significantly add more information on the action of hormones, interferons, colony-stimulating factors, and interleukins [24] together with its involvement in neurogenesis [25], glial differentiation [26] and CNS diseases [27] [28].…”

Section: Introductionmentioning

confidence: 99%

JAK-STAT Lodges in Multiple Sclerosis: Pathophysiology and Therapeutic Approach Overview

Hamid¹,

Isiyaku²,

Kalgo³

et al. 2017

OALib

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Multiple sclerosis (MS) is a complex inflammatory and demyelinating disease of central nervous system (CNS). The disease pathogenesis is not fully understood and no actual cure for the disease yet. The disease has genetic and environmental cause as fundamental factors which are identified for the disease pathogenesis so far. One of the characteristic features of the disease is inflammation cause due to activation of pro-inflammatory cells. Interference in signalling pathways such as JAK/STAT could result in physiological or pathological outcome in MS. Dysregulation of JAK/STAT signalling pathway is associated with chronic inflammatory process and immune disorders. In this review, considering the important role of JAK/STAT pathway in signal transduction of inflammatory process and immune responses in CNS, we describe the involvement of this signal transduction pathway in MS. Moreover, we consider the physiological and pathological involvement of JAK/STAT rout in neurogenesis/gliogenesis, cytokines production and as therapeutics target for managing MS.

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“…It was observed upon transduction of rodent telencephalic precursors with artificial alleles of Stat3, encoding for a gain-of-function version of this protein (Stat3c, constitutively dimerizing, however still requiring Lif stimulation for its transactivating properties), or encoding for dominant-negative versions of it (Stat3f, unable to get Y-phosphorylated, and Stat3d, unable to bind to DNA) )(Gu et al, 2005. Moreover, astrogenic properties of pStat3 were evident upon cre/loxP-mediated ablation of Stat3 in murine E14.5 cortico-cerebral NSCs (Cao et al, 2010), as well as after knock-down of Stat3 mediated by RNAi (Aberg et al, 2001;Barnabé-Heider et al, 2005;He et al, 2005). Interestingly, reduced astrogenesis caused by Stat3-LOF manipulations was often associated to an excess of neuronal differentiation (Gu et al, 2005;Cao et al, 2010).…”

Section: Transactive Pathways Modulating Astrogenesismentioning

confidence: 99%

Developmental control of cortico-cerebral astrogenesis

Mallamaci¹

2013

Int. J. Dev. Biol.

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A remarkable body of research over the last 15 years has been aimed at disentangling the cellular and molecular mechanisms which regulate murine cortico-cerebral astrogenesis. This research effort has allowed the reconstruction of the actual sizing of this process, as well as a better definition of its temporal, spatial and clonal articulation. Moreover, these investigations have shed substantial light on the cardinal molecular mechanisms governing the transition from pallial neuronogenesis to astrogenesis, as well as subsequent progress of the latter. It has turned out that proper temporal articulation of astrogenesis relies on a plethora of tightly interlaced mechanisms, which synergistically dampen astrogenesis prior to birth and promote it during peri-and postnatal life. The aim of this review is to provide a comprehensive and organic synthesis of these mechanisms, as well as a critical evaluation of their specific relevance to proper articulation of cerebral cortex astrogenesis in time and space.

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Conditional deletion of Stat3 promotes neurogenesis and inhibits astrogliogenesis in neural stem cells

Cited by 73 publications

References 27 publications

GDNF facilitates differentiation of the adult dentate gyrus-derived neural precursor cells into astrocytes via STAT3

GDNF facilitates differentiation of the adult dentate gyrus-derived neural precursor cells into astrocytes via STAT3

JAK-STAT Lodges in Multiple Sclerosis: Pathophysiology and Therapeutic Approach Overview

Developmental control of cortico-cerebral astrogenesis

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