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Relevant bibliographies by topics / Neuronal progenitors

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Academic literature on the topic 'Neuronal progenitors'

Author: Grafiati

Published: 25 May 2024

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Journal articles on the topic "Neuronal progenitors"

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Shih, Hung-Yu, Chia-Wei Chang, Yi-Chieh Chen, and Yi-Chuan Cheng. "Identification of the Time Period during Which BMP Signaling Regulates Proliferation of Neural Progenitor Cells in Zebrafish." International Journal of Molecular Sciences 24, no. 2 (2023): 1733. http://dx.doi.org/10.3390/ijms24021733.

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Bone morphogenetic protein (BMP) signaling regulates neural induction, neuronal specification, and neuronal differentiation. However, the role of BMP signaling in neural progenitors remains unclear. This is because interruption of BMP signaling before or during neural induction causes severe effects on subsequent neural developmental processes. To examine the role of BMP signaling in the development of neural progenitors in zebrafish, we bypassed the effect of BMP signaling on neural induction and suppressed BMP signaling at different time points during gastrulation using a temporally controlled transgenic line carrying a dominant-negative form of Bmp receptor type 1aa and a chemical inhibitor of BMP signaling, DMH1. Inhibiting BMP signaling from 8 hpf could bypass BMP regulation on neural induction, induce the number of proliferating neural progenitors, and reduce the number of neuronal precursors. Inhibiting BMP signaling upregulates the expression of the Notch downstream gene hairy/E(spl)-related 2 (her2). Inhibiting Notch signaling or knocking down the Her2 function reduced neural progenitor proliferation, whereas inactivating BMP signaling in Notch-Her2 deficient background restored the number of proliferating neural progenitors. These results reveal the time window for the proliferation of neural progenitors during zebrafish development and a fine balance between BMP and Notch signaling in regulating the proliferation of neural progenitor cells.

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Wang, D. D., D. D. Krueger, and A. Bordey. "Biophysical Properties and Ionic Signature of Neuronal Progenitors of the Postnatal Subventricular Zone In Situ." Journal of Neurophysiology 90, no. 4 (2003): 2291–302. http://dx.doi.org/10.1152/jn.01116.2002.

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Previous studies have reported the presence of neuronal progenitors in the subventricular zone (SVZ) and rostral migratory stream (RMS) of the postnatal mammalian brain. Although many studies have examined the survival and migration of progenitors after transplantation and the factors influencing their proliferation or differentiation, no information is available on the electrophysiological properties of these progenitors in a near-intact environment. Thus we performed whole cell and cell-attached patch-clamp recordings of progenitors in brain slices containing either the SVZ or the RMS from postnatal day 15 to day 25 mice. Both regions displayed strong immunoreactivity for nestin and neuron-specific class III β-tubulin, and recorded cells displayed a morphology typical of the neuronal progenitors known to migrate throughout the SVZ and RMS to the olfactory bulb. Recorded progenitors had depolarized zero-current resting potentials (mean more depolarized than –28 mV), very high input resistances (about 4 GΩ), and lacked action potentials. Using the reversal potential of K+ currents through a cell-attached patch a mean resting potential of –59 mV was estimated. Recorded progenitors displayed Ca2+-dependent K+ currents and TEA-sensitive-delayed rectifying K+ (KDR) currents, but lacked inward K+ currents and transient outward K+ currents. KDR currents displayed classical kinetics and were also sensitive to 4-aminopyridine and α-dendrotoxin, a blocker of Kv1 channels. Na+ currents were found in about 60% of the SVZ neuronal progenitors. No developmental changes were observed in the passive membrane properties and current profile of neuronal progenitors. Together these data suggest that SVZ neuronal progenitors display passive membrane properties and an ionic signature distinct from that of cultured SVZ neuronal progenitors and mature neurons.

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Turrero García, Miguel, José-Manuel Baizabal, Diana N. Tran, et al. "Transcriptional regulation of MGE progenitor proliferation by PRDM16 controls cortical GABAergic interneuron production." Development 147, no. 22 (2020): dev187526. http://dx.doi.org/10.1242/dev.187526.

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ABSTRACTThe mammalian cortex is populated by neurons derived from neural progenitors located throughout the embryonic telencephalon. Excitatory neurons are derived from the dorsal telencephalon, whereas inhibitory interneurons are generated in its ventral portion. The transcriptional regulator PRDM16 is expressed by radial glia, neural progenitors present in both regions; however, its mechanisms of action are still not fully understood. It is unclear whether PRDM16 plays a similar role in neurogenesis in both dorsal and ventral progenitor lineages and, if so, whether it regulates common or unique networks of genes. Here, we show that Prdm16 expression in mouse medial ganglionic eminence (MGE) progenitors is required for maintaining their proliferative capacity and for the production of proper numbers of forebrain GABAergic interneurons. PRDM16 binds to cis-regulatory elements and represses the expression of region-specific neuronal differentiation genes, thereby controlling the timing of neuronal maturation. PRDM16 regulates convergent developmental gene expression programs in the cortex and MGE, which utilize both common and region-specific sets of genes to control the proliferative capacity of neural progenitors, ensuring the generation of correct numbers of cortical neurons.

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Ruan, Xiangbin, Bowei Kang, Cai Qi, Wenhe Lin, Jingshu Wang, and Xiaochang Zhang. "Progenitor cell diversity in the developing mouse neocortex." Proceedings of the National Academy of Sciences 118, no. 10 (2021): e2018866118. http://dx.doi.org/10.1073/pnas.2018866118.

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In the mammalian neocortex, projection neuron types are sequentially generated by the same pool of neural progenitors. How neuron type specification is related to developmental timing remains unclear. To determine whether temporal gene expression in neural progenitors correlates with neuron type specification, we performed single-cell RNA sequencing (scRNA-Seq) analysis of the developing mouse neocortex. We uncovered neuroepithelial cell enriched genes such as Hmga2 and Ccnd1 when compared to radial glial cells (RGCs). RGCs display dynamic gene expression over time; for instance, early RGCs express higher levels of Hes5, and late RGCs show higher expression of Pou3f2. Interestingly, intermediate progenitor cell marker gene Eomes coexpresses temporally with known neuronal identity genes at different developmental stages, though mostly in postmitotic cells. Our results delineate neural progenitor cell diversity in the developing mouse neocortex and support that neuronal identity genes are transcriptionally evident in Eomes-positive cells.

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Findlay, Quan, Kiryu K. Yap, Annette J. Bergner, Heather M. Young, and Lincon A. Stamp. "Enteric neural progenitors are more efficient than brain-derived progenitors at generating neurons in the colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 7 (2014): G741—G748. http://dx.doi.org/10.1152/ajpgi.00225.2014.

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Gut motility disorders can result from an absent, damaged, or dysfunctional enteric nervous system (ENS). Cell therapy is an exciting prospect to treat these enteric neuropathies and restore gut motility. Previous studies have examined a variety of sources of stem/progenitor cells, but the ability of different sources of cells to generate enteric neurons has not been directly compared. It is important to identify the source of stem/progenitor cells that is best at colonizing the bowel and generating neurons following transplantation. The aim of this study was to compare the ability of central nervous system (CNS) progenitors and ENS progenitors to colonize the colon and differentiate into neurons. Genetically labeled CNS- and ENS-derived progenitors were cocultured with aneural explants of embryonic mouse colon for 1 or 2.5 wk to assess their migratory, proliferative, and differentiation capacities, and survival, in the embryonic gut environment. Both progenitor cell populations were transplanted in the postnatal colon of mice in vivo for 4 wk before they were analyzed for migration and differentiation using immunohistochemistry. ENS-derived progenitors migrated further than CNS-derived cells in both embryonic and postnatal gut environments. ENS-derived progenitors also gave rise to more neurons than their CNS-derived counterparts. Furthermore, neurons derived from ENS progenitors clustered together in ganglia, whereas CNS-derived neurons were mostly solitary. We conclude that, within the gut environment, ENS-derived progenitors show superior migration, proliferation, and neuronal differentiation compared with CNS progenitors.

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Nagler, Arnon, Hadar Arien-Zakay, Shimon Lecht, Hanan Galski, and Philip Lazarovici. "Nerve Growth Factor-Responsive Neuronal Progenitors From Human Umbilical Cord Blood." Blood 114, no. 22 (2009): 4601. http://dx.doi.org/10.1182/blood.v114.22.4601.4601.

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Abstract Abstract 4601 Background Nerve growth factor (NGF) is a well characterized neurotrophin required for the survival and differentiation of a variety of cell types in the peripheral and central nervous system. Over the last decade, many studies have demonstrated the physiological role of NGF in proliferation, differentiation and activation of different hematopoietic cells. Hematopoietic progenitors from bone marrow, umbilical cord blood and peripheral blood were found to be responsive to the actions of NGF. Furthermore, bone marrow stromal cells produce and respond to NGF during different steps of normal hematopoiesis. Results In this study, we describe a population of collagen-adherent, CD49a/b (á1/2 integrin receptors) and nestin-positive human umbilical cord blood derived progenitors. The identity of these cells was established as positive for the mesenchymal markers: CD13, CD29, CD44, CD49a,b, CD49e, CD73, CD105 and vimentin and negative for the hematopoietic markers: CD34, CD49c, CD49d, CD62e, CD62p, CD106, CD117, CD133, CD235a, HLA-DRB4 and HAS1, using Affimatrix™ human DNA chip technology, immunomagnetic sorting and Western blotting approaches. The NGF- receptor, TrkA, was found to be expressed upon isolation of these progenitors, but was gradually down-regulated upon 14 days growth in culture, as measured by mRNA, protein expression and binding properties. However, continuous presense of NGF in the culture media preserved the TrkA receptors expression. The pan-neurotrophin NGF receptor p75NTR, belonging to the TNF family of cell-death receptors, was not detected in the progenitors at any time. The effect of NGF on the cord blood progenitors global gene expression indicated highly increased expression of 170 genes, 24 and 20% of which were related to neuronal proliferation (NEK1, cyclin B1, EGR4, LGN, GATA6) or differentiation (AP2, Neurogenic differentiation factor 2, lamin B1, Ca(2+)-activated Cl- channel, Kv channel, GABA-A alpha 5 receptor, D2 dopamine receptor, neuropeptides precursor), respectively and strong reduction in the expression of 58 genes, 35% of which were hematopoiesis-related (CD7, T cell receptor alpha, interleukin 21 receptor, natural killer cell transcript 4, HLA-G, complement component1, defensin alpha1). Furthermore, upon treatment with NGF, the progenitors expressed a neuronal-like phenotype as evaluated by measurements of long neurite outgrowths and various developmental neuronal markers expression (MAP-2, NeuN neurofillament-160, beta-tubulin III, neuron specific enolase). These findings strongly suggest NGF-induced reprogramming of the cord blood derived progenitors towards neuronal differentiation commitment. The progenitors were also found to confer ∼35% neuroprotection to neurons exposed to an ischemic damage by a “bystander” effect mechanism, which includes the increased autocrine secretion of NGF and activation of TrkA receptors in the insulted neurons. Conclusions These results suggest an important role for NGF in regulating human umbilical cord blood neuronal progenitor's growth and reprogramming towards neuronal differentiation. In view of the broad spectrum of possible uses of cord blood in transplantations, we may also suggest that human umbilical cord blood and/or derived NGF-responsive progenitors may serve as a useful source of neuronal cells for cell therapy of neuropathological disorders. Disclosures: No relevant conflicts of interest to declare.

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Antel, Jack P., Josephine Nalbantoglu, and André Olivier. "Neuronal progenitors—learning from the hippocampus." Nature Medicine 6, no. 3 (2000): 249–50. http://dx.doi.org/10.1038/73076.

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Dubreuil, V., M. Hirsch, A. Pattyn, J. Brunet, and C. Goridis. "The Phox2b transcription factor coordinately regulates neuronal cell cycle exit and identity." Development 127, no. 23 (2000): 5191–201. http://dx.doi.org/10.1242/dev.127.23.5191.

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In the vertebrate neural tube, cell cycle exit of neuronal progenitors is accompanied by the expression of transcription factors that define their generic and sub-type specific properties, but how the regulation of cell cycle withdrawal intersects with that of cell fate determination is poorly understood. Here we show by both loss- and gain-of-function experiments that the neuronal-subtype-specific homeodomain transcription factor Phox2b drives progenitor cells to become post-mitotic. In the absence of Phox2b, post-mitotic neuronal precursors are not generated in proper numbers. Conversely, forced expression of Phox2b in the embryonic chick spinal cord drives ventricular zone progenitors to become post-mitotic neurons and to relocate to the mantle layer. In the neurons thus generated, ectopic expression of Phox2b is sufficient to initiate a programme of motor neuronal differentiation characterised by expression of Islet1 and of the cholinergic transmitter phenotype, in line with our previous results showing that Phox2b is an essential determinant of cranial motor neurons. These results suggest that Phox2b coordinates quantitative and qualitative aspects of neurogenesis, thus ensuring that neurons of the correct phenotype are generated in proper numbers at the appropriate times and locations.

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Mikhailov, Andrey, and Yoshiyuki Sankai. "Apoptosis in Postmortal Tissues of Goat Spinal Cords and Survival of Resident Neural Progenitors." International Journal of Molecular Sciences 25, no. 9 (2024): 4683. http://dx.doi.org/10.3390/ijms25094683.

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Growing demand for therapeutic tissue repair recurrently focusses scientists’ attention on critical assessment of postmortal collection of live cells, especially stem cells. Our study aimed to assess the survival of neuronal progenitors in postmortal spinal cord and their differentiation potential. Postmortal samples of spinal cords were obtained from human-sized animals (goats) at 6, 12, 24, 36, and 54 h after slaughter. Samples were studied by immunohistology, differentiation assay, Western blot and flow cytometry for the presence and location of GD2-positive neural progenitors and their susceptibility to cell death. TUNEL staining of the goat spinal cord samples over 6–54 h postmortem revealed no difference in the number of positive cells per cross-section. Many TUNEL-positive cells were located in the gray commissure around the central canal of the spinal cord; no increase in TUNEL-positive cells was recorded in either posterior or anterior horns of the gray matter where many GD2-positive neural progenitors can be found. The active caspase 3 amount as measured by Western blot at the same intervals was moderately increasing over time. Neuronal cells were enriched by magnetic separation with antibodies against CD24; among them, the GD2-positive neural progenitor subpopulation did not overlap with apoptotic cells having high pan-caspase activity. Apoptotic cell death events are relatively rare in postmortal spinal cords and are not increased in areas of the neural progenitor cell’s location, within measured postmortal intervals, or among the CD24/GD2-positive cells. Data from our study suggest postmortal spinal cords as a valuable source for harvesting highly viable allogenic neural progenitor cells.

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McConnell, SK, and CE Kaznowski. "Cell cycle dependence of laminar determination in developing neocortex." Science 254, no. 5029 (1991): 282–85. http://dx.doi.org/10.1126/science.254.5029.282.

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The neocortex is patterned in layers of neurons that are generated in an orderly sequence during development. This correlation between cell birthday and laminar fate prompted an examination of how neuronal phenotypes are determined in the developing cortex. At various times after labeling with [3H]thymidine, embryonic progenitor cells were transplanted into older host brains. The laminar fate of transplanted neurons correlates with the position of their progenitors in the cell cycle at the time of transplantation. Daughters of cells transplanted in S-phase migrate to layer 2/3, as do host neurons. Progenitors transplanted later in the cell cycle, however, produce daughters that are committed to their normal, deep-layer fates. Thus, environmental factors are important determinants of laminar fate, but embryonic progenitors undergo cyclical changes in their ability to respond to such cues.

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Dissertations / Theses on the topic "Neuronal progenitors"

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Hayashi, Junya. "Primate embryonic stem cell-derived neuronal progenitors transplanted into ischemic brain." Kyoto University, 2006. http://hdl.handle.net/2433/135623.

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Chapman, Heather M. "Gsx genes control the neuronal to glial fate switch in telencephalic progenitors." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1394725163.

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Larrosa, Madeleine Julie [Verfasser]. "The function of the zinc finger transcription factor Insm1 in neuronal progenitors / Madeleine Larrosa." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1219508306/34.

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Larrosa, Madeleine [Verfasser]. "The function of the zinc finger transcription factor Insm1 in neuronal progenitors / Madeleine Larrosa." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1219508306/34.

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Hyroššová, Petra. "Not to be picky: PEPCK-M ensures metabolic flexibility in cancer cells and neuronal progenitors." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/672607.

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Phosphoenolpyruvate carboxykinase (PEPCK) is an enzyme that catalyses decarboxylation of oxaloacetate to phosphoenolpyruvate and it is part of gluconeogenic/glyceroneogenic pathway. There are two known isoforms of PEPCK, the mitochondrial and the cytosolic isozyme that are catalysing chemically identical reactions, but they differ in regulation and expression pattern. Selective presence of mitochondrial isoform of this enzyme (PEPCK-M, PCK2) in all types of cancer examined and in cycling neuroprogenitors, suggests a functional relationship with the metabolic adaptations of these cells. This thesis has had as its main objectives the characterization of the role of PEPCK-M in tumour cells and in neuronal progenitor cells. Metabolism of cell in CNS is not completely elucidated yet. Here we demonstrate that Tbr2 positive neuronal progenitors are metabolically dependent on lactate, which is favouring maintenance of their undifferentiated state. Lactate as metabolite can feed anabolic pathways and sustain ATP production by its oxidation in the TCA cycle. However, essential pathways like PPP, glycerol synthesis or one carbon metabolism pathways require carbons to feed the glycolytic intermediate pool. PEPCK-M in this setting, with lactate as sole carbon source is the only known pathway to fulfil the above-mentioned anabolic requirements. By using inhibitor of PEPCK-M we were able to prove that Tbr2 positive neuronal progenitors are metabolically dependent on PEPCK-M activity and their number significantly decrease after inhibiting PEPCK-M in vitro and in vivo. PEPCK-M activity in tumour cells is necessary for survival and growth in 2D and in cultures on semi-solid agar (anchorage-independent growth), which suggests that this enzyme has a fundamental role in the survival program to cell stress. A Kaplan-Meier analysis from datasets available in the GEO database (> 5000 patients) shows that elevated PCK2 expression is significantly associated with a worse prognosis in patients with breast cancer. Despite its potential relevance for metabolic adaptations in cancer, the mechanisms responsible for its pro- survival activity are not known. Therefore, we have proposed to study these mechanisms through metabolomic analysis where we wanted to examine whether PEPCK-M feeds an alternative pathway to glucose using carbons from glutamine in an experimental model with reduced and overexpressed levels of PEPCK-M activity. We demonstrated the functionality of PEPCK-M driven cataplerosis in MCF7 cells grown under glucose deprivation by showing synthesis of serine and glycine from glutamine by observing contribution of 13C-labeled carbons from [U-13C] glutamine into these metabolites. In the absence of nutritional stress (high abundance of glucose and amino acids), the silencing of PEPCK-M induces oxidative stress and the accumulation of succinate, with the consequent induction of p21 and deficiencies in cell growth. Glutamine cataplerosis is not affected by alterations in PEPCK-M activity. However, a higher enrichment of all carbons with 13C in intermediates of the Krebs cycle (TCA cycle) suggests a reduction in flux through this pathway. Together, these data increase our understanding of metabolic adaptations in tumours and the role of PEPCK in providing alternative carbon fluxes to deal with nutritional stress. Finally, these studies allow us to propose PEPCK-M as a new target for the treatment of tumorigenic processes that will need to be validated in the future.<br>El fosfoenolpiruvato carboxiquinasa mitocondrial (PEPCK-M; PCK2) se regula transcripcionalmente por limitación de aminoácidos y por ER-estrés, de una manera dependiente de ATF4, aumentando así la supervivencia de la célula. La presencia selectiva de esta isoenzima en todos los tipos de cáncer examinado y en células neuroprogenitoras, sugiere una relación funcional con las adaptaciones metabólicas de estas células. Esta tesis ha tenido como objetivos fundamentales la caracterización del rol de la PEPCK-M en célula tumoral y en célula neuroprogenitora En cultivos neuronales, los neuroprogenitores Tbr2 positivos requieren lactato como sustrato metabólico para el mantenimiento de su fenotipo y su metabolismo. La PEPCK-M se expresa a niveles altos en este tipo celular y su actividad es necesaria para mantener la viabilidad de estos progenitores y cumplir con los requerimientos anabólicos a partir de carbonos provenientes del lactato. La actividad PEPCK-M en célula tumoral es necesaria para la supervivencia y crecimiento. A pesar de su potencial relevancia para las adaptaciones metabólicas en cáncer, no se conocen los mecanismos responsables de su actividad pro-supervivencia. Por ello, nos hemos propuesto estudiar estos mecanismos mediante análisis de metabolómica con los que hemos querido examinar si la PEPCK-M alimenta una vía alternativa a la glucosa utilizando carbonos provenientes de glutamina en un modelo experimental con niveles de actividad PEPCK-M reducidos y sobreexpresados. La contribución de carbonos marcados con 13C a partir de [U- 13C] glutamina en los productos de ramificación de glicolisis como serina y glicina, esta correlacionando directamente con los niveles de actividad PEPCK-M en condiciones de estrés nutricional (baja glucosa). La cataplerosis de glutamina no se ve afectada por alteraciones en la actividad de PEPCK-M. Sin embargo, un mayor enriquecimiento de 13C en intermediarios del ciclo de Krebs sugieren una reducción del flujo a través de esta vía. En conjunto, estos datos aumentan nuestra comprensión de las adaptaciones metabólicas en los tumores y el papel de la PEPCK en la provisión de flujos de carbono alternativas para lidiar con el estrés nutricional. Finalmente, estos estudios nos permiten proponer a la PEPCK-M como una nueva diana para el tratamiento de procesos tumorogénicos que necesitará ser validada en el futuro.

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WACLAW, RONALD RAYMOND. "MOLECULAR CONTROL OF NEURONAL DIVERSITY IN LATERAL GANGLIONIC EMINENCE PROGENITORS OF THE EMBRYONIC MOUSE TELENCEPHALON." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1130334258.

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Belmonte, Mateos Carla 1992. "Unveiling the molecular and behavioral properties of hindbrain rhombomere centers." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2022. http://hdl.handle.net/10803/673433.

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Precise regulation of neurogenesis is achieved by differentially allocating the neurogenic competence along the tissue. In the hindbrain proneural gene expression is stereotypically confined in segment boundary-adjacent regions, hence, being absent in segment centers. This segregation of proneural gene expression therefore hints rhombomere centers as a putative non-neurogenic population. In this work, we unveil their spatiotemporal molecular profile as well as one of the mechanisms involved in their maintenance as non-committed progenitors. By 4D imaging we shed light for the first time into the in vivo cell behavior this population displays. We propose this population in rhombomere centers is indeed heterogeneous as it harbors cells with different proliferative capacity.<br>La regulació precisa de la neurogènesi s’aconsegueix localitzant la competència neurogènica de manera diferencial al llarg del territori. Al cervell posterior, l’expressió de gens proneurals es restringeix a les zones adjacents a les cèl·lules de les fronteres, i per tant és absent als centres així doncs assenyalant els centres dels rombòmers com una població no neurogènica. En aquest treball, hem revelat el seu perfil molecular espai-temporal així com un dels mecanismes que manté aquestes cèl·lules com a no neurogèniques. Mitjançant imatges 4D hem aportat llum per primera vegada a l’enteniment del seu comportament cel·lular en viu, i proposem que aquesta població dels centres dels rombòmers és de fet heterogènia ja que conté cèl·lules amb diferent capacitat proliferativa.

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Tayel, Sara [Verfasser], Marius [Gutachter] Ader, and Frank [Gutachter] Buchholz. "Identifiying Casc15 as a novel regulator of progenitors’ proliferation and neuronal migration in the developing neocortex / Sara Tayel ; Gutachter: Marius Ader, Frank Buchholz." Dresden : Technische Universität Dresden, 2021. http://d-nb.info/123184616X/34.

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McLaughlin, Heather Ward. "Modeling sporadic Alzheimer's disease using induced pluripotent stem cells." Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13094355.

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Despite being the leading cause of neurodegeneration and dementia in the aging brain, the cause of Alzheimer's disease (AD) remains unknown in most patients. The terminal pathological hallmarks of abnormal protein aggregation and neuronal cell death are well-known from the post-mortem brain tissue of Alzheimer's disease patients, but research into the earliest stages of disease development is hindered by limited model systems. In this thesis, an in vitro human neuronal system was derived from induced pluripotent stem (iPS) cell lines reprogrammed from dermal fibroblasts of AD patients and age-matched controls. This allows us to investigate the cellular mechanisms of AD neurodegeneration in the human neurons of sporadic AD (SAD) patients, whose development of the disease cannot be explained by our current understanding of AD. We show that neural progenitors and neurons derived from SAD patients show an unexpected expression profile of enhanced neuronal gene expression resulting in premature differentiation in the SAD neuronal cells. This difference is accompanied by the decreased binding of the repressor element 1-silencing transcription/neuron-restrictive silencer factor (REST/NRSF) transcriptional inhibitor of neuronal differentiation in the SAD neuronal cells. The SAD neuronal cells also have increased production of \(amyloid-\beta\) and higher levels of tau protein, the main components of the plaques and tangles in the AD brain.

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Voltes, Cobo Adrià 1991. "Hindbrain boundaries : addressing the crossroad between tissue segmentation and cell fate regulation." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/665625.

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The hindbrain boundary cell population (BCP) is specified at the interface between adjacent compartments during embryonic development of the posterior brain. Hindbrain BCP is a non-neurogenic population that acts as both a signaling center and an elastic mesh that prevents cell intermingling between adjacent compartments. Remarkably, boundary cells display mechanical characteristics that emphasize the impact of tissue segmentation on boundary architecture: they display specific cell morphology and contain actomyosin cable-like structures that provide the boundaries with the tension necessary for carrying out their physical barrier role. Considering the mechanical microenvironment in the BCP and its identity specificities, we propose YAP/TAZ-TEAD activity as the molecular scaffold that underpins the crossroad between hindbrain segmentation and proliferative capacity modulation. In this work we show that mechanical stimuli in the BCP trigger YAP/TAZ-TEAD activity. In turn, this activity is responsible for transiently modulating the proliferative capacity of boundary cells, which eventually differentiate into neurons.<br>La població cel·lular de les fronteres del romboencèfal (PCF) s’especifica a la interfície entre compartiments adjacents durant el desenvolupament embrionari del cervell posterior. La PCF del romboencèfal és una població no neurogènica que actua com a centre senyalitzador i com a barrera elàstica que evita la barreja de cèl·lules entre compartiments adjacents. Cal destacar que les cèl·lules de les fronteres presenten característiques mecàniques que fan palès l’impacte de la segmentació del teixit sobre l’arquitectura de les fronteres: presenten una morfologia cel·lular específica i contenen estructures d’actomiosina de tipus cable que proporcionen a les fronteres la tensió necessària per portar a terme la funció de barrera física. Considerant el microambient mecànic a la PCF i les seves especificitats en termes d’identitat, proposem l’activitat YAP/TAZ-TEAD com la bastida molecular present a la intersecció entre la segmentació del romboencèfal i la modulació de la capacitat proliferativa. En aquesta investigació demostrem que els estímuls mecànics presents a la PCF desencadenen l’activitat YAP/TAZ-TEAD. Al seu torn, aquesta activitat és transitòriament responsable de la modulació de la capacitat proliferativa de les cèl·lules de les fronteres, les quals acabaran diferenciant-se en neurones.

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Books on the topic "Neuronal progenitors"

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Naglieri, Benedetta. Complex Regulation of Pax6 Neuronal Progenitors By Rb Family Members During Corticogenesis. [publisher not identified], 2012.

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The neuroendocrine Leydig cells and their stem cell progenitors, the pericytes. Springer, 2009.

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Arturo, Álvarez-Buylla, and García-Verdugo José Manuel, eds. Identification and characterization of neural progenitor cells in the adult mammalian brain. Springer, 2009.

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Rolfs, A. Isolation and Induction of Neuronal Progenitor Cells: Rostock Spring School 2006 Contributions, Special Issue, Neurodegenerative Diseases 2007. S Karger Pub, 2007.

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Book chapters on the topic "Neuronal progenitors"

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Zholudeva, Lyandysha V., Ying Jin, Liang Qiang, Michael A. Lane, and Itzhak Fischer. "Preparation of and Progenitors: Neuronal Production and Applications." In Neuronal Cell Culture. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1437-2_7.

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Bonner, Joseph F., Christopher J. Haas, and Itzhak Fischer. "Preparation of Neural Stem Cells and Progenitors: Neuronal Production and Grafting Applications." In Neuronal Cell Culture. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_7.

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Rex, Tonia S. "Virus-mediated Gene Delivery to Neuronal Progenitors." In Advances in Experimental Medicine and Biology. Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-74904-4_16.

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Thomaidou, Dimitra, Panagiotis K. Politis, and Rebecca Matsas. "Neurogenesis in the Central Nervous System: Cell Cycle Progression/Exit and Differentiation of Neuronal Progenitors." In Cell Cycle Regulation and Differentiation in Cardiovascular and Neural Systems. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-60327-153-0_8.

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Alt, Frederick W., Pei-Chi Wei, and Bjoern Schwer. "Recurrently Breaking Genes in Neural Progenitors: Potential Roles of DNA Breaks in Neuronal Function, Degeneration and Cancer." In Research and Perspectives in Neurosciences. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60192-2_6.

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Horie, Nobutaka. "Neural Stem Cells/Neuronal Progenitor Cells." In Cell Therapy Against Cerebral Stroke. Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56059-3_3.

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Darbinyan, Armine, Rafal Kaminski, Martyn K. White, Nune Darbinian, and Kamel Khalili. "Isolation and Propagation of Primary Human and Rodent Embryonic Neural Progenitor Cells and Cortical Neurons." In Neuronal Cell Culture. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_5.

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Luskin, M. B., T. Zigova, R. Betarbet, and B. J. Soteres. "Characterization of Neuronal Progenitor Cells of the Neonatal Forebrain." In Isolation, Characterization and Utilization of CNS Stem Cells. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-80308-6_5.

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Ocasio, Jennifer Karin. "Maintaining Cerebellar Granule Neuron Progenitors in Cell Culture." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2752-5_2.

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Falls, Douglas L., and Marla B. Luskin. "Neuronal Progenitor Cells of the Mammalian Neonatal Anterior Subventricular Zone." In Neural Development and Stem Cells. Humana Press, 2006. http://dx.doi.org/10.1385/1-59259-914-1:123.

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Conference papers on the topic "Neuronal progenitors"

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Hwang, Inah, Dongqing Cao, Do-Yeon Kim, et al. "Abstract 2481: Loss of FUBP1 impairs terminal neuronal differentiation and predisposes neural progenitors for transformation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2481.

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Lepski, Guilherme, Chary Batista, Eric Mariano, et al. "Pain Inhibition Through Transplantation of Fetal Neuronal Progenitors into the Injured Spinal Cord in Rats." In XXXII Congresso Brasileiro de Neurocirurgia. Thieme Revinter Publicações Ltda, 2018. http://dx.doi.org/10.1055/s-0038-1672636.

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Abasi, Sara, John R. Aggas, and Anthony Guiseppi-Elie. "Permissive Electroconductive Nanocomposites for Neuronal Progenitor Cells." In 2019 9th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2019. http://dx.doi.org/10.1109/ner.2019.8716893.

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Safronova, N. A., T. S. Kurkin, M. B. Shevtsov, et al. "SAMPLE PREPARATION OF A RECEPTOR ASSOCIATED WITH MULTIPLE SCLEROSIS PATHOGENESIS FOR STRUCTURAL STUDIES USING CRYOELECTRON MICROSCOPY." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-370.

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In this work, we study the GPCR class A receptor (rhodopsin-like) which is phylogenetically close to cysteinyl leukotriene and purine receptors. It is expressed in oligodendrocyte progenitor cells and regulates formation of the myelin sheath of neurons. To determine the structure of this receptor by cryoelectron microscopy, we created a stable and monomeric protein sample.

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Hollingsworth, Ethan, Dominic Julian, Fumihiro Watanabe, et al. "Interferome perturbation of human brain organoids induces progenitor and neuronal dysfunction seen in multiple sclerosis and autism (P2-3.015)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000204077.

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Wortham, Matthew, Genglin Jin, Julia Lailai Sun, Darell D. Bigner, and Hai Yan. "Abstract 3352: The medulloblastoma oncogene Otx2 enhances migration and permits ectopic proliferation of neuronal progenitor cells of the cerebellum and brainstem." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3352.

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Santos, Júlia Romano Ferreira, Érika Laís de Oliveira Silva, Iris Dutra Barbosa, Lorrane Silva Moura Dorneles, and Fernanda Guimarães Vieira. "REVISÃO DE LITERATURA: ASPECTOS MORFOLÓGICOS NEURONAIS CONGÊNITOS DESENCADEADOS PELA INFECÇÃO INTRA-UTERINA POR ZIKA VÍRUS." In I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3216.

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Introdução: Por Zika vírus (ZIKV) entende-se o patógeno arboviral pertencente ao gênero Flavivirus, notório por ser transmitido vetorialmente por artrópodes do gênero Aedes - dentre eles o Aedes aegypti - e hábil a desencadear a infecção sistêmica Zika. Foi diagnosticado documentalmente, no Brasil, em maio de 2015, por métodos biomoleculares sistematizados por pesquisadores da Universidade Federal da Bahia. O progressivo aumento das notificações relacionadas ao nascimento de crianças com microcefalia, no Nordeste, exigiu atenção do Ministério da Saúde, a fim de investigar correlações fisiopatológicas reportadas, tais como acometimentos oculares e deficiências cognitivas, com alterações morfológicas em recém-nascidos com ZIKV. Objetivo: Revisar estudos sobre impactos congênitos neuronais em crianças infectadas verticalmente pelo ZIKV para compreender eventuais alterações morfológicas. Material e Métodos: Trata-se de uma Revisão Integrativa de Literatura, realizada a partir da leitura íntegra de 23 publicações científicas, escritas em Português e em Inglês entre 2016 e 2021, acerca das disfunções morfológicas embrionárias desencadeadas pela infecção por ZIKV. Tal elegibilidade deu-se pelo levantamento em Bases de Dados (Scopus, PubMed, Scielo e Portal CAPES) com cruzamento dos Descritores Zika virus, Embryology e Congenital Abnormalities. Resultados: A infecção fetal pelo ZIKV ainda não é totalmente esclarecida e, apesar de estudos sugerirem que o vírus seja capaz de driblar a imunoproteção placentária, ainda há um hiato quanto à influência viral em anomalias congênitas. Entretanto, já foi comprovado que o ZIKV induz efeitos citopáticos por desencadear lesões histológicas no citotrofoblasto ao subverter o sistema imunológico placentário, com tropismo por Macrófagos, via expressão do sfRNA viral. Alguns estudos identificaram antígenos virais em Células Progenitoras de Sinais Neuronais (hNPCs), sendo tal conteúdo viral hábil a modular negativamente a neurogênese por induzir a apoptose a partir da regulação, via mecanismos ainda obscuros, da expressão gênica. Particularmente, as hNPCs superexpressam Receptores AXL, capazes de viabilizarem o egresso intracelular do ZIKV e de mediarem vias de sinalização supressoras da resposta imunitária inata, magnificando a neurovirulência. Conclusão: A infecção congênita por ZIKV induz alterações morfológicas que lesam o Sistema Nervoso Fetal pela depleção das hNPCs corticais, resultando em malformações neurológicas.

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Van Dyke, William S., Ozan Akkus, and Eric Nauman. "Murine Osteochondral Stem Cells Express Collagen Type I More Strongly on PDMS Substrates Than on Tissue Culture Plastic." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14272.

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The discovery of the multipotent lineage of mesenchymal stem cells has dawned a new age in tissue engineering, where an autologous cell-seeded scaffold can be implanted into different therapeutic sites. Mesenchymal stem cells have been reported to differentiate into numerous anchorage-dependent cell phenotypes, including neurons, adipocytes, myoblasts, chondrocytes, tenocytes, and osteoblasts. A seminal work detailing that mesenchymal stem cells can be directed towards differentiation of different cell types by substrate stiffness alone [1] has led to numerous studies attempting to understand how cells can sense the stiffness of their substrate [2–3] Substrate stiffness has been shown to be an inducer of stem cell differentiation. MSCs on extremely soft substrates (250 Pa), similar to the stiffness of bone marrow, became quiescent but still retained their multipotency [4]. Elastic substrates in the stiffness range of 34 kPa revealed MSCs with osteoblast morphology, and osteocalcin along with other osteoblast markers were expressed [1]. However, osteogenesis has been found to increase on much stiffer (20–80 kPa) [5–6] (400 kPa) [7] as well as much softer substrates (75 Pa) [8]. Overall, cells have increased projected cell area and proliferation on stiffer substrates, leading to higher stress fiber formation. This study seeks to understand if the stiffness of the substrate has any effect on the differentiation potential of osteochondral progenitor cells into bone cells, using an in vitro dual fluorescent mouse model.

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Maire, Cecile L., Shakti H. Ramkissoon, and Keith L. Ligon. "Abstract 3304: Conditional Pten loss in Olig2 expressing neural stem/progenitor cells results in massive myelination and disruption of the neuronal differentiation in the absence of neoplasia." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3304.

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Zhang, Z., A. Lei, L. Xu, et al. "PO-277 Postmitotic neuron-like differentiation of cancer cells suggests that cancer cells have the properties of neural precursor/progenitor cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.308.

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Reports on the topic "Neuronal progenitors"

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Carvey, Paul M. Cytokine Induction of Dopamine Neurons from Progenitor Cells. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada391417.

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