Isolation of neural stem/progenitor cells by using EGF/FGF1 and FGF1B promoter-driven green fluorescence from embryonic and adult mouse brains

Lee, Dong Hoon; Hsu, Yi‐Chao; Chung, Yu‐Fen; Hsiao, Chao-Yang; Chen, Suliang; Chen, Mei‐Shu; Lin, Hua‐Kuo; Chiu, Ing‐Ming

doi:10.1016/j.mcn.2009.04.010

Cited by 35 publications

(48 citation statements)

References 108 publications

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“…NSCs were isolated and cultured according to the method described previously [39,40]. Briefly, mouse embryos at day 11.5 were collected from the pregnant FVB strain mice and placed in basal medium (a 1:1 mixture of Dulbecco's modified Eagle's medium high glucose/Ham's F12 medium [D/F12, Gibco] containing 100 units/ml penicillin and 100 mg/ml streptomycin).…”

Section: Isolation and Culture Of Nscsmentioning

confidence: 99%

Induction and regulation of differentiation in neural stem cells on ultra-nanocrystalline diamond films

et al. 2010

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Section: Isolation and Culture Of Nscsmentioning

confidence: 99%

Induction and regulation of differentiation in neural stem cells on ultra-nanocrystalline diamond films

et al. 2010

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“…The average daily intake of acrylamide for adults is approximately 0.5 mg/kg body weight; children may have two to three times more intake than adults (18,38,55 exposed people at a lifelong intake of 0.08 mg/kg body weight/day (47). Rodriguez-Ramiro et al have shown that smaller doses of acrylamide can act as toxicant when administered in long-term exposure (48).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Neurosphere Formation in Neural Stem/Progenitor Cells by Acrylamide

et al. 2015

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Previous studies showed that transplantation of cultured neural stem/progenitor cells (NSPCs) could improve functional recovery for various neurological diseases. This study aims to develop a stem cell-based model for predictive toxicology of development in the neurological system after acrylamide exposure. Treatment of mouse (KT98/F1B-GFP) and human (U-1240 MG/F1B-GFP) NSPCs with 0.5 mM acrylamide resulted in the inhibition of neurosphere formation (definition of self-renewal ability in NSPCs), but not inhibition of cell proliferation. Apoptosis and differentiation of KT98 (a precursor of KT98/F1B-GFP) and KT98/F1B-GFP are not observed in acrylamide-treated neurospheres. Analysis of secondary neurosphere formation and differentiation of neurons and glia illustrated that acrylamide-treated KT98 and KT98/F1B-GFP neurospheres retain the NSPC properties, such as self-renewal and differentiation capacity. Correlation of acrylamide-inhibited neurosphere formation with cell-cell adhesion was observed in mouse NSPCs by live cell image analysis and the presence of acrylamide. Protein expression levels of cell adhesion molecules [neural cell adhesion molecule (NCAM) and N-cadherin] and extracellular signal-regulated kinases (ERK) in acrylamide-treated KT98/F1B-GFP and U-1240 MG/F1B-GFP neurospheres demonstrated that NCAM decreased and phospho-ERK (pERK) increased, whereas expression of N-cadherin remained unchanged. Analysis of AKT (protein kinase B, PKB)/b-catenin pathway showed decrease in phospho-AKT (p-AKT) and cyclin D1 expression in acrylamide-treated neurospheres of KT98/F1B-GFP. Furthermore, PD98059, an ERK phosphorylation inhibitor, attenuated acrylamide-induced ERK phosphorylation, indicating that pERK contributed to the cell proliferation, but not in neurosphere formation in mouse NSPCs. Coimmunoprecipitation results of KT98/F1B-GFP cell lysates showed that the complex of NCAM and fibroblast growth factor receptor 1 (FGFR1) is present in the neurosphere, and the amount of this complex decreases after acrylamide treatment. Our results reveal that acrylamide inhibits neurosphere formation through the disruption of the neurosphere architecture in NSPCs. The downregulation of cell-cell adhesion resulted from decreasing the levels of NCAM as well as the formation of NCAM/ FGFR complex.

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“…Neural stem cells have been isolated from brain tissues according to the NSC-specific cell surface marker CD133 and NSCspecific genes, such as Sox1, Sox2, nestin, and FGF1 [54,55]. Thus, NSCs can be isolated using such approaches and then cultured to form neurospheres, which are indicators of self-renewal.…”

Section: Isolation and Characterization Of Neural Stem Cellsmentioning

confidence: 99%

“…Furthermore, the FGF-1B promoter-driven GFP reporter (F1B-GFP) (USA patent No. 6984 518; 7045 678; and 7745 214) was used to isolate NSCs from human [55] and mouse brains [54,55]. The F1B-GFP-selected NSCs exhibited significant repair efficacy in the damaged sciatic nerves of paraplegic rats.…”

Section: Isolation and Characterization Of Neural Stem Cellsmentioning

confidence: 99%

Neural Stem Cells and Induced Neurons for Nerve Injury Repair

Hsu¹,

Chen²,

Hsu³

et al. 2015

J Stem Trans Bio

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Cell transplantation can relieve the symptoms of or even reverse neurodegenerative diseases and repair nerve injuries. Fibroblast growth factor 1 promotes neuronal survival and stimulates axonal growth. A combination of fibroblast growth factor 1 and cell-based therapy is promising for nerve repair. Developers of future cell-based treatment should consider several key concerns: (1) the source of cells should be autologous, (2) consistent methods and protocols for cell isolation should be used, (3) the treatment should be tested in suitable animal models, and (4) the microenvironment of cells implanted should be optimally characterized. In addition, developing high temporal and spatial resolution images for cell tracking is crucial for evaluating the efficacy of cell transplantation. In this paper, we summarize recent progress in cellular reprogramming, such as induced neural stem cells and induced neurons, and the development of future cell-based therapy for peripheral nerve and spinal cord injury that includes conduits and growth factors. Fibroblast Growth Factor 1 for Nerve Injury RepairIn total, 22 mammalian fibroblast growth factors (FGFs) exist, grouped into seven subfamilies on the basis of differences in sequence homology and phylogeny. Notably, FGF1 and FGF2 share sequential and structural similarities and belong to the FGF1 subfamily [1]. The FGF ligands execute diverse functions by binding and activating the FGF receptor (FGFR) family of tyrosine kinase receptors with heparan sulfate proteoglycans. In total, four FGFR genes (FGFR1-FGFR4) encode receptors consisting of three extracellular immunoglobulin domains (D1-D3), a single-pass transmembrane domain, and a cytoplasmic tyrosine kinase domain [2]. Several FGFR isoforms exist because of exon skipping that removes the D1 domain and/or the acid box in FGFR1-FGFR4 [3]. Alternative splicing in the second half of the D3 domain of FGFR1-FGFR3 yields b (FGFR1b-FGFR3b) and c (FGFR1c-FGFR3c) isoforms that have distinct FGFbinding specificities [4] and are predominantly present in epithelial and mesenchymal cells, respectively. Each FGF binds to epithelial or mesenchymal FGFRs, with the exception of FGF1, which activates both spliced isoforms [3].The involvement of FGF signaling in human diseases has been thoroughly documented. Deregulated FGF signaling can contribute to pathological conditions through gain-or loss-of-function mutations in the FGFRs. Because both Fgf1 −/− and Fgf1mice are fertile and apparently normal [5], the physiological roles of FGF1 and FGF2 remain to be explored. However, FGF1 and FGF2 likely play a physiological role in the maintenance of the vascular tone because FGF1 and FGF2 administration lowers the blood pressure in rats [6] and can restore the nitric oxide synthase activity in spontaneously hypertensive rats [7]. In addition, blood vessels isolated from Fgf2 −/− mice exhibit a reduced response to vasoconstrictors. Although Fgf2 −/− mice had hypotension caused by reduced smooth muscle contractility [8], their blood pressu...

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Isolation of neural stem/progenitor cells by using EGF/FGF1 and FGF1B promoter-driven green fluorescence from embryonic and adult mouse brains

Cited by 35 publications

References 108 publications

Induction and regulation of differentiation in neural stem cells on ultra-nanocrystalline diamond films

Induction and regulation of differentiation in neural stem cells on ultra-nanocrystalline diamond films

Inhibition of Neurosphere Formation in Neural Stem/Progenitor Cells by Acrylamide

Neural Stem Cells and Induced Neurons for Nerve Injury Repair

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