SVZa neural stem cells differentiate into distinct lineages in response to BMP4

Liu, Shiyong; Zhang, Zhiyuan; Song, Yechun; Kejun, Qiu; Zhang, Kecheng; An, Ning; Zhou, Zheng; Cai, Wenqin; Yang, Hui

doi:10.1016/j.expneurol.2004.07.015

Cited by 36 publications

(21 citation statements)

References 62 publications

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“…In each embryonic stage, NPC proliferation or differentiation is mostly regulated by locally produced or peripherally circulating soluble paracrine factors such as growth factors (e.g. basic fibroblast growth factor (b-FGF) and epidermal growth factor (EGF)) and cytokines as well as several autocrine factors such as bone morphogenic protein-4 (BMP4), interleukin 6, glycosylated cystatin C, and insulin-like growth factors (Eccleston et al, 1991;Liu et al, 2004;WisletGendebien et al, 2004). Although glial progenitors are known to arise from NPCs predominantly at a delay on neurogenesis, the underlying spatiotemporal regulatory mechanisms of proliferation and differentiation of glial progenitors are not yet defined.…”

Section: Introductionmentioning

confidence: 99%

PACAP/PAC1 autocrine system promotes proliferation and astrogenesis in neural progenitor cells

Nishimoto

Furuta

Aoki

et al. 2006

Glia

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The Pituitary adenylate cyclase-activating peptide (PACAP) ligand/type 1 receptor (PAC1) system regulates neurogenesis and gliogenesis. It has been well established that the PACAP/PAC1 system induces differentiation of neural progenitor cells (NPCs) through the Gs-mediated cAMP-dependent signaling pathway. However, it is unknown whether this ligand/receptor system has a function in proliferation of NPCs. In this study, we identified that PACAP and PAC1 were highly expressed and co-localized in NPCs of mouse cortex at embryonic day 14.5 (E14.5) and found that the PACAP/PAC1 system potentiated growth factor-induced proliferation of mouse cortical NPCs at E14.5 via Gq-, but not Gs-, mediated PLC/IP3-dependent signaling pathway in an autocrine manner. Moreover, PAC1 activation induced elongation of cellular processes and a stellate morphology in astrocytes that had the bromodeoxyuridine (BrdU)-incorporating ability of NPCs. Consistent with this notion, we determined that the most BrdU positive NPCs differentiated to astrocytes through PAC1 signaling. These results suggest that the PACAP/PAC1 system may play a dual role in neural/glial progenitor cells not only differentiation but also proliferation in the cortical astrocyte lineage via Ca2+-dependent signaling pathways through PAC1.

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Section: Introductionmentioning

confidence: 99%

PACAP/PAC1 autocrine system promotes proliferation and astrogenesis in neural progenitor cells

Nishimoto

Furuta

Aoki

et al. 2006

Glia

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“…9 Liu et al reported that low concentrations of BMP4 promoted the proliferation of anterior subventricular zone (SVZa) NSCs, whereas high concentrations of BMP4 inhibited this proliferation, and BMP4 enhanced neuron commitment before 4 days but inhibited it after 4 days. 10 Recent studies have revealed that NSCs and GSCs share many common signal pathways, 11,12 and GSCs are considered to have originated from transformed NSCs. 13,14 Thus, whether BMP4 is involved in GSC regulation is unclear and needs further investigation.…”

Section: Introductionmentioning

confidence: 99%

Bone Morphogenetic Protein 4 Inhibits Cell Proliferation and Induces Apoptosis in Glioma Stem Cells

Zhou

Sun

Wang

et al. 2011

Cancer Biotherapy and Radiopharmaceuticals

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Glioma stem cells (GSCs), which are originated from transformed neural stem cells, are tumor-initiating cells of glioma, the most common primary malignant neoplasm of the central nervous system. Extensive studies have shown that bone morphogenetic protein 4 (BMP4) plays an important role in the differentiation and proliferation of neural stem cells. To seek the functions and mechanisms of BMP4 in GSCs, GSCs isolated from U87 human glioma cells by using vincristine were exposed to BMP4 protein. This study shows that BMP4 inhibited U87 GSC proliferation (p < 0.01) via downregulation of cyclin D1 level and promoted GSC apoptosis through induction of Bax expression and inhibition of Bcl-2 and Bcl-xL levels. Thus, these results indicate a new approach of GSC-based glioma treatment.

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“…For example, BMP4 promotes proliferation of NSCs cultured from the anterior SVZ at low concentration, but inhibits proliferation at high concentration. BMP4 enhanced neuron commitment of these cells at an early stage but inhibited it at a later stage [102]. Interactions between BMP and other signaling pathways including Wnt/β-catenin, basic helix–loop-helix (bHLH) and hypoxia-inducible factor-1α (HIF-1α) are essential for appropriate developmental outcomes [103], [104].…”

Section: Human Gliomas and Bmp4mentioning

confidence: 99%

Therapeutic Potential for Bone Morphogenetic Protein 4 in Human Malignant Glioma

Best

Mania-Farnell

et al. 2017

Neoplasia

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Human glioma, in particular, malignant forms such as glioblastoma exhibit dismal survival rates despite advances in treatment strategies. A population of glioma cells with stem-like features, glioma cancer stem-like cells (GCSCs), contribute to renewal and maintenance of the tumor cell population and appear responsible for chemotherapeutic and radiation resistance. Bone morphogenetic protein 4 (BMP4), drives differentiation of GCSCs and thus improves therapeutic efficacy. Based on this observation it is imperative that the clinical merits of BMP4 in treating human gliomas should be addressed. This article reviews BMP4 signaling in central nervous system development and in glioma tumorigenesis, and the potential of this molecule as a treatment target in human gliomas. Further work needs to be done to determine if distinct lineages of GCSCs, associated with different glioma sub-classifications, proneural, neural, classical and mesenchymal, differ in responsiveness to BMP4 treatment. Additionally, interaction among BMP4 and cell matrix, tumor-vascular molecules and microglial immune cells also needs to be investigated, as this will enhance our knowledge about the role of BMP4 in human glioma and lead to the identification and/or development of novel therapeutic approaches that improve treatment outcomes of these devastating tumors.

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SVZa neural stem cells differentiate into distinct lineages in response to BMP4

Cited by 36 publications

References 62 publications

PACAP/PAC1 autocrine system promotes proliferation and astrogenesis in neural progenitor cells

PACAP/PAC1 autocrine system promotes proliferation and astrogenesis in neural progenitor cells

Bone Morphogenetic Protein 4 Inhibits Cell Proliferation and Induces Apoptosis in Glioma Stem Cells

Therapeutic Potential for Bone Morphogenetic Protein 4 in Human Malignant Glioma

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