Gotowe bibliografie tematyczne / Neuronal differentiation

Gotowa bibliografia na temat „Neuronal differentiation”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 września 2023

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Artykuły w czasopismach na temat "Neuronal differentiation"

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Kawaguchi, Tsutomu, Hiroaki Yokoyama, Masaru Inoue, Akio Ichikura, Masashige Onizuka i Masao Kishikawa. "A Case of Pineocytoma with Neuronal Differentiation". Japanese Journal of Neurosurgery 4, nr 2 (1995): 180–84. http://dx.doi.org/10.7887/jcns.4.180.

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Léopold, Pierre. "Neuronal Differentiation". Cell 119, nr 1 (październik 2004): 4–5. http://dx.doi.org/10.1016/j.cell.2004.09.024.

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Miyahara, Hiroaki, Manabu Natsumeda, Junichi Yoshimura, Yukihiko Fujii, Akiyoshi Kakita, Yasushi Iwasaki i Mari Yoshida. "MBRS-32. TOPOISOMERASE II β INDUCES NEURONAL, BUT NOT GLIAL, DIFFERENTIATION IN MEDULLOBLASTOMA". Neuro-Oncology 22, Supplement_3 (1.12.2020): iii404. http://dx.doi.org/10.1093/neuonc/noaa222.546.

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Abstract BACKGROUND We previously reported that Gli3, which was a downstream molecule of Sonic Hedgehog signal, induced neuronal and/or glial differentiation in some types of medulloblastoma (desmoplastic/nodular medulloblastoma and medulloblastoma with extensive nodularity), and patients of medulloblastoma with neuronal differentiation showed favorable prognosis, but those with glial differentiation tended to show miserable prognosis (Miyahara H, Neuropathology, 2013). This time, we focused on Topoisomerase II β (Top2β), which was reported to induce neuronal differentiation and inhibit glial differentiation, and examined the expression of Top2β in medulloblastomas with neuronal and glial differentiations. METHODS We assessed the expression of Top2β, NeuN, and GFAP using triple fluorescent immunostaining method in medulloblastoma samples with both neuronal and glial differentiations. Furthermore, the expression of Top2β, H3K4me2, and H3K27me3 were also assessed, because Top2βwas positively or negatively regulated by H3K4me2 and H3K27me3, respectively. RESULTS Many large nuclei in the nodules, in which differentiated cells were seen, was visualized by Top2β. The Top2β signals were seen in NeuN+ cells but not GFAP+ cells. H3K4me2 signals were visualized in Top2β+ large nuclei, but H3K27me3 and NeuN+ large nuclei were distributed independently. CONCLUSIONS These results indicate that Top2β may be a molecule associated with neuronal, but not glial, differentiation of medulloblastoma cells. Drugs targeting histone modification enzymes such as EZH2 inhibitors are possible therapeutic targets as a differentiation-inducing therapy for medulloblastoma.
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Pérez, María Julia, Tomas Roberto Carden, Paula Ayelen dos Santos Claro, Susana Silberstein, Pablo Martin Páez, Veronica Teresita Cheli, Jorge Correale i Juana M. Pasquini. "Transferrin Enhances Neuronal Differentiation". ASN Neuro 15 (styczeń 2023): 175909142311707. http://dx.doi.org/10.1177/17590914231170703.

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Although transferrin (Tf) is a glycoprotein best known for its role in iron delivery, iron-independent functions have also been reported. Here, we assessed apoTf (aTf) treatment effects on Neuro-2a (N2a) cells, a mouse neuroblastoma cell line which, once differentiated, shares many properties with neurons, including process outgrowth, expression of selective neuronal markers, and electrical activity. We first examined the binding of Tf to its receptor (TfR) in our model and verified that, like neurons, N2a cells can internalize Tf from the culture medium. Next, studies on neuronal developmental parameters showed that Tf increases N2a survival through a decrease in apoptosis. Additionally, Tf accelerated the morphological development of N2a cells by promoting neurite outgrowth. These pro-differentiating effects were also observed in primary cultures of mouse cortical neurons treated with aTf, as neurons matured at a higher rate than controls and showed a decrease in the expression of early neuronal markers. Further experiments in iron-enriched and iron-deficient media showed that Tf preserved its pro-differentiation properties in N2a cells, with results hinting at a modulatory role for iron. Moreover, N2a-microglia co-cultures revealed an increase in IL-10 upon aTf treatment, which may be thought to favor N2a differentiation. Taken together, these findings suggest that Tf reduces cell death and favors the neuronal differentiation process, thus making Tf a promising candidate to be used in regenerative strategies for neurodegenerative diseases.
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FUKUSHIMA, Takeo, Masamichi TOMONAGA, Toshio SAWADA i Hiroshi IWASAKI. "Pineocytoma with Neuronal Differentiation". Neurologia medico-chirurgica 30, nr 1 (1990): 63–68. http://dx.doi.org/10.2176/nmc.30.63.

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Tateno, M., W. Ukai, M. Yamamoto, E. HashimotAo, H. Ikeda i T. Saito. "ALCOHOL AND NEURONAL DIFFERENTIATION." Alcoholism: Clinical & Experimental Research 28, Supplement (sierpień 2004): 69A. http://dx.doi.org/10.1097/00000374-200408002-00376.

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Rösner, H., M. Al-Aqtum i H. Rahmann. "Gangliosides and neuronal differentiation". Neurochemistry International 20, nr 3 (kwiecień 1992): 339–51. http://dx.doi.org/10.1016/0197-0186(92)90048-v.

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Lamar, E., C. Kintner i M. Goulding. "Identification of NKL, a novel Gli-Kruppel zinc-finger protein that promotes neuronal differentiation". Development 128, nr 8 (15.04.2001): 1335–46. http://dx.doi.org/10.1242/dev.128.8.1335.

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The proneural basic helix-loop-helix proteins play a crucial role in promoting the differentiation of postmitotic neurons from neural precursors. However, recent evidence from flies and frogs indicates that additional factors act together with the proneural bHLH proteins to promote neurogenesis. We have identified a novel zinc finger protein, neuronal Kruppel-like protein (NKL), that positively regulates neurogenesis in vertebrates. NKL is expressed in Xenopus primary neurons and in differentiating neuronal precursors in the intermediate zone of the mouse and chick neural tube. In frog embryos, NKL is induced by overexpression of Neurogenin (Ngn), arguing that NKL is downstream of the proneural determination genes. Our results show that NKL and a NKL/VP16 fusion protein promote differentiation of neuronal precursors in the embryonic chick spinal cord. Following in ovo misexpression of NKL, neuroepithelial cells exit the cell cycle and differentiate into neurons. Similarly, NKL/VP16 induces extra primary neurons in frogs and upregulates expression of the neural differentiation factors, Xath3 and MyT1, as well as the neuronal markers, N-tubulin and elrC. Our findings establish NKL as a novel positive regulator of neuronal differentiation and provide further evidence that non-bHLH transcription factors function in the neuronal differentiation pathway activated by the vertebrate neuronal determination genes.
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Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, Stefan Putz, Kevin Achberger, Leonhard Linta, Stefan Liebau, Tobias M. Boeckers i Andreas M. Grabrucker. "Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells". Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/3760702.

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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation.
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Erin, Nuray, i Özkan Ulusoy. "Differentiation of neuronal from non-neuronal Substance P". Regulatory Peptides 152, nr 1-3 (styczeń 2009): 108–13. http://dx.doi.org/10.1016/j.regpep.2008.10.006.

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Rozprawy doktorskie na temat "Neuronal differentiation"

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Rocha, Joana Fernandes da. "Understanding APP-dependent neuronal differentiation". Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/7389.

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Mestrado em Biomedicina Molecular
Amyloid Precursor Protein (APP) is a type 1 membrane protein that suffers proteolytic cleavages and has been implicated in roles such as cell adherence, survival, migration and differentiation. Although a role in neuritogenesis has been attributed to APP, some contradictory results have been reported regarding the benefits of knocking-down or overexpressing APP. Further, while the addition of the APP proteolytic sAPP (secreted APP) fragment to the cell medium enhances neuritogenesis, the amount of cellular APP and other APP fragments may be deleterious for this process. Further, preliminary work from the Neuroscience laboratory of the Center for Cell Biology indicated that pAPP (APP phosphorylated at the S655 residue) can potentially be crucial in APPmediated neuronal differentiation, for example by increasing APP cleavage to its biological fragment sAPP or APP binding to specific signal transducers. In this work, the capacity of APP and pAPP to mediate neuronal differentiation was tested, in the initial period of retinoic acid (RA)-induced SH-SY5Y cells differentiation. These neuroblastoma cells are a well documented neuronal-like cell model used in neuronal differentiation studies. Several molecular tools were used, including wild-type and phosphomutants APP-GFP. The evaluation of differentiation included neuritogenic output analysis by bright field and epifluorescence microscopy, using various approaches. Namely scoring the number of differentiated cells and performing morphometric analyses of transfected cells and of the all cellular population. The levels of APP and medium secreted sAPP, and of cytoskeleton-related proteins and posttranslational modifications, such as MAP2, Acetylated Tubulin and Actin were also quantified by Western blot analysis, and related to the morphological parameters. Additionally, the potential role of AICD in APP-mediated neuronal differentiation was inferred from pharmacologic assays, where its generation is inhibited. Together the results obtained show that APP, sAPP and AICD modulate neuritogenesis in a complex and well-ordered manner. While long-term increases in APP can be detrimental to neuronal-like differentiation, in an AICD-dependent manner, short-term increases benefit this process in an APP S655 phosphorylation dependent manner, potentially involving sAPP secretion and specific cytoskeleton rearrangements.
A Proteína Precursora de Amilóide de Alzheimer (PPA) é uma proteína membranar tipo 1 sujeita a processamento proteolítico que tem sido associada a funções como adesão celular, sobrevivência, migração e diferenciação. Apesar de lhe terem sido atribuídas funções na neuritogénese, os dados experimentais obtidos até à data que envolveram modulação dos níveis da PPA revelam-se contraditórios. De facto, enquanto a adição do fragmento PPA secretado (PPAs) ao meio celular favorece a neuritogénese, a quantidade de PPA celular e de outros fragmentos da PPA poderão já não constituir um benefício para este processo. Adicionalmente, dados preliminares do laboratório de Neurociências do Centro de Biologia Celular sugerem que a PPAp (PPA fosforilada na S655) poderá ser fundamental na diferenciação neuronal mediada pela PPA, nomeadamente por aumentar a proteólise da PPA a PPAs ou a ligação da PPA a sinais de transdução específicos. No presente trabalho, avaliou-se a capacidade da PPA e PPAp em mediar o período inicial de diferenciação neuronal induzida por ácido retinóico. Para tal recorreu-se a células de neuroblastoma SH-SY5Y, um modelo celular do tipo neuronal bem estabelecido para estudos de diferenciação. Adicionalmente, várias ferramentas moleculares, como PPA-GFP selvagem e fosfomutantes foram usadas. A avaliação da diferenciação incluiu a análise de vários parâmetros neuritogénicos por microscopia de luz (de campo claro e de fluorescência), nomeadamente monitorização de células diferenciadas e análises morfométricas das células transfectadas e da população geral. Os níveis de PPA e PPAs, e de proteínas relacionadas com citosqueleto e suas modificações pós-traducionais (MAP2, Tubulina Acetilada e Actina) também foram quantificados. Além do mais, a influência do DIP na diferenciação neuronal dependente de PPA foi avaliada usando um composto farmacológico para inibir a sua produção. De um modo geral, os resultados obtidos demonstram que a PPA, PPAs e DIP modulam a neuritogénese de um modo complexo e ordenado. Enquanto a indução de níveis altos de expressão de PPA (48h) podem ser detrimentais para a diferenciação tipo-neuronal, de uma forma dependente de DIP, induções mais breves (24h) beneficiam este processo de um modo dependente da fosforilação na S655, potencialmente envolvendo a secreção de PPA e rearranjos específicos do citosqueleto.
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Unsworth, Harriet Christina. "Connexins in neuronal and epidermal differentiation". Thesis, Queen Mary, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429065.

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Gore, S. "Neuronal differentiation markers in basal cell carcinoma". Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445574/.

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Basal cell carcinoma (BCC) is the most common skin cancer in humans. The demonstration of genetic and protein alterations has, so far, had limited correlation with either biological behaviour or histological classification of these tumours. It was observed that Glil-overexpressing keratinocytes express elevated levels of genes known to be associated with neuronal development, including p-tubulin III, GAP-43, Arc and neurofilament. It was proposed that these genes may similarly be overexpressed in BCCs and that different levels of expression may be present in different BCC subtypes Immunohistochemistry of BCCs demonstrated that neuronal differentiation marker proteins are expressed in BCCs, but that this expression is significantly reduced in tumours that behave aggressively. Elevated neuronal differentiation marker gene expression was shown in BCCs. Again, expression was more prominent in tumour types that behave indolently. Results were obtained for tumour samples processed by laser capture microdissection, needle microdissection and homogenised tissue. Expression of neuronal differentiation marker genes in Gli-overexpressing keratinocytes was examined by semi-quantitiative PCR. Neuronal differentiation marker expression was associated with GUI and GH2 over-expression in some cases {P-tubulin III and Arc). GUI and GH2 also promoted the expression of each other in a positive-feedback loop. Expression of these markers was examined in archival tumours for which the clinical outcome was known in terms of recurrence. In completely excised tumours P-tubulin III was significantly reduced in tumours that went on to subsequently recur. Other markers were not expressed in significantly different amounts. In summary, I have shown that expression of markers associated with neuronal development is a feature of Basal Cell carcinoma, and that the expression of these markers correlates strongly with the tumour histological subtype but only weakly with tumour recurrence. More work will be required to discover further alterations in BCC molecular biology that impact significantly on tumour behaviour.
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Higginbotham, Holden Richard. "Polarity regulation during neuronal migration and differentiation". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3315121.

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Thesis (Ph. D.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed Aug. 4, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 150-172).
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CECI, CLAUDIA. "Effect of nickel exposure on neuronal differentiation". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/203180.

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Nickel, a known occupational/environmental hazard, may cross the placenta and reach appreciable concentrations in various fetal organs, including the brain. The aim of this study was to investigate whether nickel interferes with the process of neuronal differentiation. For this purpose we have utilized the human teratocarcinoma-derived NTera2/D1 cell line (NT2 cells), which represent a widely recognized model system of human neural progenitors. Following a 4 week treatment with retinoic acid (10 μM), NT2 cells terminally differentiate into neurons which recapitulate many features of human fetal neurons. The continuous exposure of the differentiating NT2 cells to a not cytotoxic nickel concentration (10 μM) increased the expression of specific neuronal differentiation markers such as Microtubule Associated Protein 2 (MAP2) and Neural Cell Adhesion Molecule (NCAM). Nickel exposure also increased the expression of Hypoxia-Inducible-Factor-1α (HIF-1α) and induced the activation of the AKT/PKB kinase pathway, as shown by the increase of phosphorylated AKT/PKB kinase and P(Ser-9)-GSK-3β, the inactive form of glycogen synthase kinase-3β (GSK-3β). Stabilization of Hypoxia-Inducible-Factor 1α (HIF-1α) appears to be correlated to a reduced expression of the class III histone deacetylase SIRT1, known to be involved in neural differentiation. Intriguingly, by the end of the fourth week of differentiation, the expression of tyrosine hydroxylase (TH) protein, a marker of dopaminergic neurons, was lower in nickel-treated than in control cultures. Thus, likely by partially mimicking hypoxic conditions, the exposure to a not-cytotoxic nickel concentration appears to alter the process of neuronal differentiation and hinder the expression of the dopaminergic neuronal phenotype. Taken together, these results suggest that nickel, by altering normal brain development, may increase susceptibility to neuro-psychopathology later in life. Great part of this work has been recently published in Neurotoxicology (Ceci C., Barbaccia M.L., Pistritto G. A not cytotoxic nickel concentration alters the expression of neuronal differentiation markers in NT2 cells. Neurotoxicology. 2015 Jan 19;47C:47-53).
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Hein, Paul. "A role for C/EBP[beta] in neuronal differentiation and neuronal regeneration /". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100623.

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Both the differentiation of cortical neurons during development and the regeneration of neurons following peripheral nerve injury are characterized by an increasing expression of axonal proteins such as Talpha1 alpha-tubulin. The mechanisms that regulate the expression of Talpha1 alpha-tubulin and other neuronal genes during differentiation and regeneration are poorly understood. The proximal promoter region of the Talpha1 alpha-tubulin gene contains putative binding sites for the C/EBP family of transcription factors, which is implicated in the regulation of genes in many differentiating cell types or in cells responding to stress. This thesis consists in defining the role of C/EBP family members in the induction of the Talpha1 alpha-tubulin gene in the early differentiation and in the regeneration of neurons. Specifically, the results presented here suggest that C/EBP family members bind to and transactivate the Talpha1 alpha-tubulin minimal promoter and that the Talpha1 alpha-tubulin promoter region that is responsive to C/EBP family members also contains neuronal differentiation and regeneration response elements.
Cortical progenitor cell fate involves collaborations between cell-intrinsic factors and extracellular cue-activated signalling pathways. Similarly, the activity of C/EBP family members is regulated by cell-intrinsic factors and by the extrinsically activated Erk 1/2-C/EBP signalling pathway in several differentiating non-neuronal cells. Here we present evidence of an analogous function for C/EBP family members in neurogenesis. The results presented in this thesis show that (1) inhibition of MEK (upstream of Erk 1/2) or inhibition of C/EBP family members blocks cortical progenitor neurogenesis; (2) inhibition of C/EBP family members promotes CNTF-induced astrogenesis; and (3) forced expression of a C/EBPbeta mutant (that is, a mimic of its Erk 1/2-RSK phosphorylated form) enhances the expression of neuron-specific genes such as Talpha1 alpha-tubulin.
Neuronal regeneration involves the re-activation of some development-associated genes such as Talpha1 alpha-tubulin and GAP-43. To further define the role of C/EBP family members in the transcription of the Talpha1 alpha-tubulin gene in neurons during regeneration, we crossed transgenic mice that express the beta-galactosidase gene under the control of the Talpha1 alpha-tubulin minimal promoter (Talpha1MP:nLacZ) with mice that carry a null mutation for either C/EBPbeta or C/EBPdelta. The results of facial nerve crush experiments conducted on these hybrid mice show that C/EBPbeta plays a role in the transcriptional activation of the Talpha1 alpha-tubulin minimal promoter following neuronal injury. Injury-induced mRNA expression for either Talpha1 alpha-tubulin or GAP-43 was not noticeably affected by the absence of C/EBPbeta. This suggests that C/EBPbeta-independent mechanisms also play a role in neuronal regeneration.
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Lochter, André. "Control of neuronal differentiation by extracellular matrix constituents /". [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10325.

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De, las Heras Rachel, i n/a. "Neuronal Differentiation: A Study Into Differential Gene Expression". Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040225.161725.

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Neuronal differentiation encompasses an elaborate developmental program which until recently was difficult to study in vitro. The advent of several cell lines able to differentiate in culture proved to be the turning point for gaining an understanding of molecular neuroscience. In particular the olfactory epithelium provides an attractive tool with which to investigate fundamental questions relating to neuronal differentiation, as it displays a unique capacity to regenerate and to retain a neurogenetic potential from its genesis and throughout adult life. The coordinated regulation of gene expression is fundamental to the control of neuronal differentiation. In order to reveal active processes at the molecular level and to dissect key components of molecular pathways, differential gene expression studies provide a foundation for the elucidation of dynamic molecular mechanisms. This thesis identified genes involved in neuronal differentiation by utilising a clonal olfactory receptor neuronal cell line (OLF442). Gene expression levels were identified using differential display and oligonucleotide array technology before and after serum deprivation. Differential display revealed two kinases whose expression levels were elevated during the differentiation of OLF442, identified as focal adhesion kinase (FAK) related non-kinase (FRNK) and mammalian ste20 like (MST)2 kinase. Furthermore, analysis of the oligonucleotide array data confirmed the expression of genes involved in altering presentation of extracellular matrix molecules, in mediating cytoskeletal rearrangements, and in ceasing the cell cycle, supporting the use of OLF442 as a model for studying differentiation. The differentiation of OLF442 results from the synchronisation of multiple transduction cascades and cellular responses as evidenced by the microarray data. A protein that can synchronise such signalling is the non-receptor protein tyrosine kinase, FAK. Thus the finding of the endogenous FAK inhibitor FRNK by differential display was intriguing as there was no difference in the expression level of FAK induced by differentiation, contrasting that of FRNK. This induced FRNK expression was derived autonomously as it was not responsive to the caspase-3 inhibitor, DEVD-CHO. This is particularly pertinent since the primary role of FRNK is to act as an inhibitor of FAK by competing with its substrates and reducing the phosphorylation of both FAK and its associated proteins. Differential display also revealed the upregulation of another kinase, which had 90% homology with rat MST2 kinase within the 3' UTR. Both mouse MST2 kinase (sequence submitted to GenBank, accession number AY058922) and the closely related family member MST1 kinase were sequenced and cloned. Moreover, evidence to support an autonomously expressed carboxyl-terminal domain of MST2 kinase is presented in Chapter 3 and provides a unique way in which MST2 may regulate its own activity. To further understand the role of MST in neuronal differentiation, a series of stable OLF442 transfections (with mutant and wild-type MST constructs) were carried out. MST was localised with cytoplasmic structures that may represent actin stress fibres, indicating a potential cytoskeletal role during neuronal differentiation. This indicated that MST1 may play a role in the morphological processes involved in neuronal differentiation. The identification of two kinases by differential display provided the motivation to understand the cellular context of OLF442 and to determine the phosphorylation status of the mitogen-activated protein kinase (MAPK) signalling cascades. Differentiation of OLF442 induced high-level phosphorylation of a putative B-Raf isoform, MEK2 and ERK1/2. Interestingly, there was a switch between preferential phosphorylation of MEK1 in undifferentiated OLF442 to preferential phosphorylation of MEK2 following differentiation. SAPK/JNK was also phosphorylated, as was the transcription factor c-Jun, which is a common substrate of both the ERK and SAPK/JNK signalling modules. The mapping of the cellular context of differentiating OLF442 has identified a promising model of a novel MAPK module. This consists of FAK signalling through Rap1 to ERK providing sustained activation, which is buffered or terminated by the expression of the endogenous FAK inhibitor FRNK. Furthermore, MST kinase could potentially play a role in regulating the cytoskeletal re-arrangements that are necessary for neuronal differentiation. MST kinase may signal transiently via the SAPK pathway to provide concomitant activation of c-Jun that is required for neuronal differentiation. An understanding of the gene expression pattern of the normal neuronal differentiation program allows a greater understanding of potential developmental aberrations. This could provide an opportunity for therapies to be conceived, while understanding the complexity of neuronal determination could also provide opportunities for stem cell transplantation.
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Marote, Ana Maria Franco Aveiro. "The effects of piezoelectric polymers on neuronal differentiation". Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/11630.

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Mestrado em Biomedicina Molecular
O crescimento de neurites é crucial para o desenvolvimento neuronal, bem como para a plasticidade e reparação na fase adulta. Após uma lesão neuronal, o sucesso da reparação é determinando pelas propriedades plásticas constitutivas dos neurónios afetados e pelo seu potencial de regeneração, que é influenciado por sinais externos físicos (ex.: cicatriz glial) e químicos (ex.: moléculas inibitórias). Recentemente, o desenvolvimento de materiais à nano-escala, que interagem com os sistemas biológicos a nível molecular, prometem revolucionar o tratamento das lesões do Sistema Nervoso Central e Periférico. Os scaffolds de nanomateriais podem suportar e promover o crescimento de neurites e consequentemente, intervir nas complexas interações moleculares que ocorrem a após o dano neuronal, entre as células e o seu ambiente extracelular. Vários estudos têm demonstrado que os materiais piezoeléctricos, que geram carga elétrica em resposta ao stress mecânico, podem ser usados para a preparação de scaffolds eletricamente carregados que devem influenciar o comportamento celular. Este estudo centrou-se nos efeitos dos materiais baseados em PLLA (ácido poli (L – láctico)) sob a forma de filmes, nanofibras orientadas aleatória e alinhadamente, e da sua polarização, na diferenciação neuronal. A linha celular de neuroblastoma (SH-SY5Y) foi utilizada para avaliar o efeito dos materiais-baseados em PLLA na adesão, viabilidade, morfologia celular, bem como na diferenciação tipo-neuronal. A análise proteómica baseada em espectrometria de massa das células cultivadas em nanofibras de PLLA foi também efetuada. Os neurónios corticais embriónicos foram seguidamente utilizados para avaliar os efeitos das nanofibras de PLLA alinhadas e da sua polarização no crescimento de neurites. Nesta análise, descobrimos que os materiais de PLLA parecem inibir parcialmente a proliferação celular, enquanto promovem a diferenciação, alterando os níveis das proteínas que intervêm nestes processos. Ocorrem alterações significativas do citoesqueleto, particularmente ao nível do citoesqueleto de actina, que não induzem mas parecem potenciar o crescimento de neurites sob exposição a um sinal extracelular como o ácido retinóico. Este efeito parece ser particularmente evidente para as nanofibras de PLLA alinhadas, que induzem efeitos intermédios na restruturação do citoesqueleto. Em geral, a polarização das amostras de PLLA tem efeitos benéficos na proliferação celular e potencia o crescimento de neurites, particularmente nos neurónios. Acreditamos que as nanofibras de PLLA alinhadas serão um bom scaffold para regeneração neuronal, uma vez que mimetiza o ambiente mecânico natural das células. Contudo, futuras experiências in vitro e in vivo são necessárias para comprovar a eficácia deste potencial scaffold.
Neuritic growth is crucial for neural development, as well as for adaptation and repair in adulthood. Upon neuronal injury, the successful neuritic regrowth is determined by the constitutive plastic properties of neurons and by their regenerative potential, which is influenced by physical (e.g. glial scar) and chemical (e.g. inhibitory molecules) extrinsic cues. Recently, the development of nanometer-scale materials, which can interact with biological systems at a molecular level, provide hope to revolutionize the treatment of central and peripheral nervous system injuries. Nanomaterial scaffolds can support and promote neuritic outgrowth and consequently, take part in the complex molecular interactions between cells and their extracellular environment after neuronal injury. Several studies have shown that piezoelectric materials, which generate electrical charge in response to mechanical strain, may be used to prepare bioactive electrically charged scaffolds that may influence cell behavior. This study focused on the effects of PLLA (poly-L-lactic acid) – based materials in the form of films, random and aligned nanofibers, and of their polarization, on neuronal-like and neuronal differentiation. The neuroblastoma SH-SY5Y cell line was used to evaluate the effect of PLLA – based materials on cellular adhesion, viability, morphology and neuron-like differentiation. Mass spectrometry-based proteomic analysis of cells grown on PLLA nanofibers was also conducted. Primary embryonic cortical neurons were further used to evaluate the effect of PLLA aligned nanofibers and their polarization on neuritic outgrowth. In this analysis, we found that PLLA materials seem to partially inhibit cell proliferation, while promoting neuronal differentiation, altering the levels of proteins that intervene in these processes. Dramatic cytoskeleton remodeling occurs, particularly at the actin cytoskeleton level, which does not induce but may potentiate neuritic outgrowth upon exposure to an extracellular cue, such as Retinoic Acid. This effect seems to be particularly evident for PLLA aligned nanofibers, which induce intermediate effects in the cytoskeleton remodeling. In general, polarization of the PLLA polymers has beneficial effects on cell proliferation and potentiates the neuritic outgrowth, particularly in neurons. We believe that polarized PLLA aligned nanofibers would be a good scaffold for neuronal regeneration, since it mimics the natural mechanical cell environment and enhances neuritic outgrowth. However, further in vitro and in vivo investigations are required to prove the efficacy of this potential scaffold.
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De, las Heras Rachel. "Neuronal Differentiation: A Study Into Differential Gene Expression". Thesis, Griffith University, 2003. http://hdl.handle.net/10072/367735.

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Neuronal differentiation encompasses an elaborate developmental program which until recently was difficult to study in vitro. The advent of several cell lines able to differentiate in culture proved to be the turning point for gaining an understanding of molecular neuroscience. In particular the olfactory epithelium provides an attractive tool with which to investigate fundamental questions relating to neuronal differentiation, as it displays a unique capacity to regenerate and to retain a neurogenetic potential from its genesis and throughout adult life. The coordinated regulation of gene expression is fundamental to the control of neuronal differentiation. In order to reveal active processes at the molecular level and to dissect key components of molecular pathways, differential gene expression studies provide a foundation for the elucidation of dynamic molecular mechanisms. This thesis identified genes involved in neuronal differentiation by utilising a clonal olfactory receptor neuronal cell line (OLF442). Gene expression levels were identified using differential display and oligonucleotide array technology before and after serum deprivation. Differential display revealed two kinases whose expression levels were elevated during the differentiation of OLF442, identified as focal adhesion kinase (FAK) related non-kinase (FRNK) and mammalian ste20 like (MST)2 kinase. Furthermore, analysis of the oligonucleotide array data confirmed the expression of genes involved in altering presentation of extracellular matrix molecules, in mediating cytoskeletal rearrangements, and in ceasing the cell cycle, supporting the use of OLF442 as a model for studying differentiation. The differentiation of OLF442 results from the synchronisation of multiple transduction cascades and cellular responses as evidenced by the microarray data. A protein that can synchronise such signalling is the non-receptor protein tyrosine kinase, FAK. Thus the finding of the endogenous FAK inhibitor FRNK by differential display was intriguing as there was no difference in the expression level of FAK induced by differentiation, contrasting that of FRNK. This induced FRNK expression was derived autonomously as it was not responsive to the caspase-3 inhibitor, DEVD-CHO. This is particularly pertinent since the primary role of FRNK is to act as an inhibitor of FAK by competing with its substrates and reducing the phosphorylation of both FAK and its associated proteins. Differential display also revealed the upregulation of another kinase, which had 90% homology with rat MST2 kinase within the 3 ΠUTR. Both mouse MST2 kinase (sequence submitted to GenBank, accession number AY058922) and the closely related family member MST1 kinase were sequenced and cloned. Moreover, evidence to support an autonomously expressed carboxyl-terminal domain of MST2 kinase is presented in Chapter 3 and provides a unique way in which MST2 may regulate its own activity. To further understand the role of MST in neuronal differentiation, a series of stable OLF442 transfections (with mutant and wild-type MST constructs) were carried out. MST was localised with cytoplasmic structures that may represent actin stress fibres, indicating a potential cytoskeletal role during neuronal differentiation. This indicated that MST1 may play a role in the morphological processes involved in neuronal differentiation. The identification of two kinases by differential display provided the motivation to understand the cellular context of OLF442 and to determine the phosphorylation status of the mitogen-activated protein kinase (MAPK) signalling cascades. Differentiation of OLF442 induced high-level phosphorylation of a putative B-Raf isoform, MEK2 and ERK1/2. Interestingly, there was a switch between preferential phosphorylation of MEK1 in undifferentiated OLF442 to preferential phosphorylation of MEK2 following differentiation. SAPK/JNK was also phosphorylated, as was the transcription factor c-Jun, which is a common substrate of both the ERK and SAPK/JNK signalling modules. The mapping of the cellular context of differentiating OLF442 has identified a promising model of a novel MAPK module. This consists of FAK signalling through Rap1 to ERK providing sustained activation, which is buffered or terminated by the expression of the endogenous FAK inhibitor FRNK. Furthermore, MST kinase could potentially play a role in regulating the cytoskeletal re-arrangements that are necessary for neuronal differentiation. MST kinase may signal transiently via the SAPK pathway to provide concomitant activation of c-Jun that is required for neuronal differentiation. An understanding of the gene expression pattern of the normal neuronal differentiation program allows a greater understanding of potential developmental aberrations. This could provide an opportunity for therapies to be conceived, while understanding the complexity of neuronal determination could also provide opportunities for stem cell transplantation
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Książki na temat "Neuronal differentiation"

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E, Rodriguez-Boulan, Nelson W. J i Keystone Meeting on Epithelial and Nueronal Cell Polarity and Differentiation (1993 : Tamarron, Colo.), red. Epithelial and neuronal cell polarity and differentiation. Cambridge [England]: Company of Biologists Ltd., 1993.

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Marty, Shankland, i Macagno Eduardo R, red. Determinants of neuronal identity. San Diego: Academic Press, 1992.

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Zheng, Chaogu. Genetic Basis of Neuronal Subtype Differentiation in Caenorhabditis elegans. [New York, N.Y.?]: [publisher not identified], 2015.

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Kandror, Elena. Modeling the Transcriptional Landscape of in vitro Neuronal Differentiation and ALS Disease. [New York, N.Y.?]: [publisher not identified], 2019.

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Loeb, David Mark. The role of Trk and secondary signaling molecules in NGF-mediated neuronal differentiation. [New York]: [Columbia University], 1993.

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Ulrich, Henning. Perspectives of Stem Cells: From tools for studying mechanisms of neuronal differentiation towards therapy. Dordrecht: Springer Science+Business Media B.V., 2010.

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H, Yu Albert C., red. Neuronal-astrocytic interactions: Implications for normal and pathological CNS function. Amsterdam: Elsevier, 1992.

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Herrera, Esperanza Meléndez, Bryan V. Phillips-Farfán i Gabriel Gutiérrez Ospina. Endothelial cell plasticity in the normal and injured central nervous system. Boca Raton: CRC Press/Taylor & Francis, 2015.

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Kevin, Hunt R., red. Cellular and molecular differentiation. Orlando: Academic Press, 1987.

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Tan, Glenn Christopher. The Dual Role of Notch Signaling During Motor Neuron Differentiation. [New York, N.Y.?]: [publisher not identified], 2012.

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Części książek na temat "Neuronal differentiation"

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Tobet, S. A., i T. O. Fox. "Sex Differences in Neuronal Morphology Influenced Hormonally throughout Life". W Sexual Differentiation, 41–83. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-2453-7_2.

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Magavi, Sanjay S., i Jeffrey D. Macklis. "Immunocytochemical Analysis of Neuronal Differentiation". W Neural Stem Cells, 345–52. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-133-8_26.

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Datta, Indrani, Debanjana Majumdar, Kavina Ganapathy i Ramesh R. Bhonde. "Stem Cells and Neuronal Differentiation". W Stem Cell Therapy for Organ Failure, 71–101. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2110-4_5.

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Darbinian, Nune. "Cultured Cell Line Models of Neuronal Differentiation: NT2, PC12". W Neuronal Cell Culture, 23–33. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_3.

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Roque, Cláudio Gouveia, i Christine E. Holt. "Tctp in Neuronal Circuitry Assembly". W Results and Problems in Cell Differentiation, 201–15. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_10.

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Darbinian, Nune. "Cultured Cell Line Models of Neuronal Differentiation: , , and SK-N-MC". W Neuronal Cell Culture, 25–38. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1437-2_3.

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Appel, Bruce, i Ajay Chitnis. "Neurogenesis and Specification of Neuronal Identity". W Results and Problems in Cell Differentiation, 237–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46041-1_12.

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Bassell, Gary J., i Robert H. Singer. "Neuronal RNA Localization and the Cytoskeleton". W Results and Problems in Cell Differentiation, 41–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-540-40025-7_3.

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Feizi, T. "Gangliosides as Autoantigens and Differentiation Antigens". W Gangliosides and Modulation of Neuronal Functions, 409–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_36.

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López-Sánchez, Noelia, María C. Ovejero-Benito, Lucía Borreguero i José M. Frade. "Control of Neuronal Ploidy During Vertebrate Development". W Results and Problems in Cell Differentiation, 547–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19065-0_22.

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Streszczenia konferencji na temat "Neuronal differentiation"

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Previtera, Michelle L., Mason Hui, Malav Desai, Devendra Verma, Rene Schloss i Noshir A. Langrana. "Neuronal Precursor Cell Proliferation on Elastic Substrates". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53246.

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Numerous stem cells therapies have been studied for the replacement of damaged neurons due to spinal cord injury. Our laboratory’s goal is to design an implantable platform for spinal cord neuron (SCN) proliferation and differentiation in order to replace damaged neurons in the injured spinal cord. Based on previous literature, we suspect we can promote neuronal precursor cell (NPC) proliferation and differentiation utilizing elastic matrices.
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Liu, Chun, Seungik Baek i Christina Chan. "The Complementary Effect of Mechanical and Chemical Stimuli on the Neural Differentiation of Mesenchymal Stem Cells". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80131.

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Mesenchymal stem cells (MSCs), derived from bone marrow stroma, are a promising source for tissue repair and regeneration, due to their excellent abilities for proliferation and multipotent differentiation. While accumulated evidences during the past decade have shown that MSCs are able to differentiate into osteoblasts, chondrocytes, myoblasts and adipocytes, more recent research suggest their potential in neuronal differentiation [1]. Chemical stimuli, including growth factors, hormones, and other regulatory molecules, are used traditionally to direct MSC differentiation. Our group has previously shown that the intracellular second messenger, cAMP, is able to initiate early phase neuron-like morphology changes and late phase neural differentiation in MSCs [2]. Studies using chemical stimuli alone, however, have shown limited success in differentiating MSCs to mature neurons, thereby suggesting other factors are necessary for this process. In recent years, interest has grown on the impact of mechanical stimulation, such as stiffness, surface topography, and mechanical stretching, on cell fate decision [3].
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Kim, Jeong Hee, i Ishan Barman. "Quantifying the differentiation of 50B11 dorsal root ganglion cells using quantitative phase imaging". W CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/cleo_at.2023.atu4q.5.

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The immortalized dorsal root ganglion (DRG) neuron cell lines are promising sensory neuron models, with particular applicability to drug development. Here, we quantitatively assess morphological changes due to forskolin-augmented neuronal differentiation using quantitative phase imaging.
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Kleiman, Ross, Michelle Previtera, Sharan Parikh, Devendra Verma, Rene Schloss i Noshir Langrana. "The Effects of Extracellular Matrix Proteins and Stiffness on Neuronal Cell Adhesion". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53596.

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Spinal cord injuries have spurred research interests in finding ways to repair or replace damaged neurons. We are looking to find novel ways to promote proliferation and differentiation of stem cells in order to replace damaged spinal cord neurons. While previous studies have shown that the mechanical properties of the cellular environment influence proliferation and differentiation, these studies have only been performed on polyacrylamide and agarose gels (1, 2). Collagen gels provide the opportunity to promote neuronal precursor cell (NPCs) proliferation and differentiation in a more natural environment by utilizing the mechanical properties of the gel. In this study, we examine the effects of 2D collagen matrices of varying stiffness on proliferation and differentiation of rat, spinal cord NPCs in order to create a more biocompatible tissue-engineered platform.
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Li, Lulu, Alexander Davidovich, Jennifer Schloss, Uday Chippada, Rene Schloss, Noshir Langrana i Martin Yarmush. "Control of Neural Lineage Differentiation in an Alginate Encapsulation Microenvironment via Cellular Aggregation". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206496.

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Cell replacement therapies, which utilize renewable stem cell sources, hold tremendous potential to treat a wide range of degenerative diseases. Although many studies have established techniques to successfully differentiate stem cells into different mature cell lineages, their practicality is limited by the lack of control during the differentiation process and low yields of differentiated cells. In order to address these issues, we have previously established a murine embryonic stem cell alginate-poly-L-lysine microencapsulation differentiation system [1]. We demonstrated that ES cell differentiation could be mediated by cell-cell aggregation in the encapsulation microenvironment. We have demonstrated that both cell aggregation and hepatocyte functions, such as urea and albumin secretions, as well as increased expression of cytokeratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression [2]. In the present studies, we assessed the feasibility of inducing neuronal lineage differentiation in the alginate microenvironment by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system. We demonstrated decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and glial fibrillary acidic protein (GFAP). In addition, we demonstrated that, by blocking the cell aggregation using anti-E-cadherin antibody, encapsulated cells increased neuronal marker expression at a later stage of the encapsulation, even in the absence of retinoic acid. In conjunction with the mechanical and physical characterizations of the alginate crosslinking network, we show that 2.2% alginate concentration is most conducive to neuronal differentiation from embryonic stem cells in the presence of retinoic acid.
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Chen, Chi-Shuo, Catherine Le, Sushant Soni, Eric Y.-T. Chen i Wei-Chun Chin. "Silk-carbon nanotube composite for stem cell neuronal differentiation". W 2011 IEEE 4th International Nanoelectronics Conference (INEC). IEEE, 2011. http://dx.doi.org/10.1109/inec.2011.5991795.

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Li, Lulu, Rene Schloss, Noshir Langrana i Martin Yarmush. "Effects of Encapsulation Microenvironment on Embryonic Stem Cell Differentiation". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192587.

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Pluripotent embryonic stem cells represent a promising renewable cell source to generate a variety of differentiated cell types. Although many investigators have described techniques to effectively differentiate stem cells into different mature cell lineages, their practicality is limited by the absence of large scale processing consideration and low yields of differentiated cells. Previously we have established a murine embryonic stem cell alginate-poly-l-lysine microencapsulation differentiation system. The three-dimensional alginate microenvironment maintains cell viability, is conducive to ES cell differentiation to hepatocyte lineage cells, and maintains differentiated cellular function. In the present work, we demonstrate that hepatocyte differentiation is mediated by cell-cell aggregation in the encapsulation microenvironment. Both cell aggregation and hepatocyte functions, such as urea and albumin secretion, as well as increased expression of cytokaratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression. Furthermore, by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system, we demonstrate decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and GFAP. Therefore, as a result of capsule parameter and microenvironment manipulation, we are capable of targeting cellular differentiation to both endodermal and ectodermal cell lineages.
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Liu, Mingli, Koichi Inoue i Zhi-gang Xiong. "Abstract 4625: ASIC1 regulates neuronal differentiation of neuroblastoma through Notch signaling pathway". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4625.

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Wagner, Omer, Alexander K. Winkel, Eva Kreysing i Kristian Franze. "Multimodal imaging using combined Optical Fourier Ptychographic Microscopy and Atomic Force Microscopy for biological measures". W CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.atu5i.3.

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We present a platform that perform live imaging using Fourier Ptychographic Microscopy co-localised with Atomic Force Microscopy. This specially fit emerging research on cellular biological processes regulated by tissue mechanics, including neuronal growth and stem-cell differentiation.
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Liu, Mingli, Koichi Inoue, An Zhou i Zhigang Xiong. "Abstract B29: ASIC1 impacts Notch signaling pathway in the neuronal differentiation of neuroblatoma". W Abstracts: Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 13-16, 2015; Atlanta, Georgia. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7755.disp15-b29.

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