Journal articles: 'Human neuroblast'

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Hanics, János, Edit Szodorai, Giuseppe Tortoriello, Katarzyna Malenczyk, Erik Keimpema, Gert Lubec, Zsófia Hevesi, et al. "Secretagogin-dependent matrix metalloprotease-2 release from neurons regulates neuroblast migration." Proceedings of the National Academy of Sciences 114, no. 10 (February 21, 2017): E2006—E2015. http://dx.doi.org/10.1073/pnas.1700662114.

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The rostral migratory stream (RMS) is viewed as a glia-enriched conduit of forward-migrating neuroblasts in which chemorepulsive signals control the pace of forward migration. Here we demonstrate the existence of a scaffold of neurons that receive synaptic inputs within the rat, mouse, and human fetal RMS equivalents. These neurons express secretagogin, a Ca2+-sensor protein, to execute an annexin V-dependent externalization of matrix metalloprotease-2 (MMP-2) for reconfiguring the extracellular matrix locally. Mouse genetics combined with pharmacological probing in vivo and in vitro demonstrate that MMP-2 externalization occurs on demand and that its loss slows neuroblast migration. Loss of function is particularly remarkable upon injury to the olfactory bulb. Cumulatively, we identify a signaling cascade that provokes structural remodeling of the RMS through recruitment of MMP-2 by a previously unrecognized neuronal constituent. Given the life-long presence of secretagogin-containing neurons in human, this mechanism might be exploited for therapeutic benefit in rescue strategies.

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Puglianiello, A., D. Germani, P. Rossi, and S. Cianfarani. "IGF-I stimulates chemotaxis of human neuroblasts. Involvement of type 1 IGF receptor, IGF binding proteins, phosphatidylinositol-3 kinase pathway and plasmin system." Journal of Endocrinology 165, no. 1 (April 1, 2000): 123–31. http://dx.doi.org/10.1677/joe.0.1650123.

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SH-SY5Y human neuroblastoma cells express IGF receptors, IGFs and IGF binding proteins (IGFBPs), and provide a model for studying the role of the IGF system in human neuronal development. We investigated the effect of IGF-I and des(1-3)IGF-I on the motility of SH-SY5Y cells by a cell migration assay based on the assessment of the number of cells which migrated across 8 microm pore size membranes and around an agarose drop. IGF-I and des(1-3)IGF-I stimulated neuroblast chemotaxis in a dose-dependent manner. Treatment of cells with these agents for 24 h resulted in a significant increase (IGF-I by 70% and des(1-3)IGF-I by 90%; P<0. 0001) in cell motility relative to control conditions. Addition of monoclonal antibody against type 1 IGF receptor (alpha-IR3), significantly (P<0.05) reduced the cell motility induced by IGF-I (by 30%) and des(1-3)IGF-I (by 70%). Wortmannin, a specific inhibitor of phosphatidylinositol (PI)-3 kinase intracellular signalling, also reduced the IGF-stimulated cell migration (by over 40%, P<0.01), indicating a key role of the PI-3 kinase pathway in mediating the IGF effect on neuroblast migration. Finally, cell treatment with plasminogen (PLG) markedly enhanced neuroblast migration (by over 200%, P<0.01), whereas incubation with the PLG inhibitor 4-(2-aminoethyl)-benzenesulphonyl fluoride reduced cell motility (by 80%, P<0.01), thus suggesting an involvement of PLG-dependent IGFBP proteolysis in the regulation of neuroblast motility. In conclusion, IGF-I is a potent stimulator of neuroblast migration through the activation of type 1 IGF receptor and the PI-3 kinase intracellular pathway. IGFBPs and the plasmin system seem to play a role in cell motility, although the nature and the extent of their involvement has yet to be elucidated.

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Chen, Jiao, and Zhonghui Guan. "Function of Oncogene Mycn in Adult Neurogenesis and Oligodendrogenesis." Molecular Neurobiology 59, no. 1 (October 8, 2021): 77–92. http://dx.doi.org/10.1007/s12035-021-02584-7.

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AbstractHuman MYCN is an oncogene amplified in neuroblastoma and many other tumors. Both human MYCN and mouse Mycn genes are important in embryonic brain development, but their functions in adult healthy nerve system are completely unknown. Here, with Mycn-eGFP mice and quantitative RT-PCR, we found that Mycn was expressed in specific brain regions of young adult mice, including subventricular zone (SVZ), subgranular zone (SGZ), olfactory bulb (OB), subcallosal zone (SCZ), and corpus callosum (CC). With immunohistochemistry (IHC), we found that many Mycn-expressing cells expressed neuroblast marker doublecortin (DCX) and proliferation marker Ki67. With Dcx-creER and Mki67-creER mouse lines, we fate mapped Dcx-expressing neuroblasts and Mki67-expressing proliferation cells, along with deleting Mycn from these cells in adult mice. We found that knocking out Mycn from adult neuroblasts or proliferating cells significantly reduced cells in proliferation in SVZ, SGZ, OB, SCZ, and CC. We also demonstrated that the Mycn-deficient neuroblasts in SGZ matured quicker than wild-type neuroblasts, and that Mycn-deficient proliferating cells were more likely to survive in SVZ, SGZ, OB, SCZ, and CC compared to wild type. Thus, our results demonstrate that, in addition to causing tumors in the nervous system, oncogene Mycn has a crucial function in neurogenesis and oligodendrogenesis in adult healthy brain.

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Kapur, R. P., C. Yost, and R. D. Palmiter. "Aggregation chimeras demonstrate that the primary defect responsible for aganglionic megacolon in lethal spotted mice is not neuroblast autonomous." Development 117, no. 3 (March 1, 1993): 993–99. http://dx.doi.org/10.1242/dev.117.3.993.

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The lethal spotted (ls) mouse has been used as a model for the human disorder Hirschsprung's disease, because as in the latter condition, ls/ls homozygotes are born without ganglion cells in their terminal colons and, without surgical intervention, die early as a consequence of intestinal obstruction. Previous studies have led to the conclusion that hereditary aganglionosis in ls/ls mice occurs because neural crest-derived enteric neuroblasts fail to colonize the distal large intestine during embryogenesis, perhaps due to a primary defect in non-neuroblastic mesenchyme rather than migrating neuroblasts themselves. In this investigation, the latter issue was addressed directly, in vivo, by comparing the distributions of ls/ls and wild-type neurons in aggregation chimeras. Expression of a transgene, D beta H-nlacZ, in enteric neurons derived from the vagal neural crest, was used as a marker for ls/ls enteric neurons in chimeric mice. In these animals, when greater than 20% of the cells were wild-type, the ls/ls phenotype was rescued; such mice were neither spotted nor aganglionic. In addition, these ‘rescued’ mice had mixtures of ls/ls and wild-type neurons throughout their gastrointestinal systems including distal rectum. In contrast, mice with smaller relative numbers of wild-type cells exhibited the classic ls/ls phenotype. The aganglionic terminal bowel of the latter mice contained neither ls/ls nor wild-type neurons. These results confirm that the primary defect in ls/ls embryos is not autonomous to enteric neuroblasts, but instead exists in the non-neuroblastic mesenchyme of the large intestine.

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Sarnat, H. B., P. G. Barth, and K. Shishikura. "EPENDYMAL ABNORMALITIES IN NEUROBLAST MIGRATORY DISORDERS OF THE HUMAN FETAL BRAIN." Journal of Neuropathology and Experimental Neurology 52, no. 3 (May 1993): 317. http://dx.doi.org/10.1097/00005072-199305000-00228.

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Zohar, Keren, Elyad Lezmi, Tsiona Eliyahu, and Michal Linial. "Ladostigil Attenuates Induced Oxidative Stress in Human Neuroblast-like SH-SY5Y Cells." Biomedicines 9, no. 9 (September 17, 2021): 1251. http://dx.doi.org/10.3390/biomedicines9091251.

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A hallmark of the aging brain is the robust inflammation mediated by microglial activation. Pathophysiology of common neurodegenerative diseases involves oxidative stress and neuroinflammation. Chronic treatment of aging rats by ladostigil, a compound with antioxidant and anti-inflammatory function, prevented microglial activation and learning deficits. In this study, we further investigate the effect of ladostigil on undifferentiated SH-SY5Y cells. We show that SH-SY5Y cells exposed to acute (by H2O2) or chronic oxidative stress (by Sin1, 3-morpholinosydnonimine) induced apoptotic cell death. However, in the presence of ladostigil, the decline in cell viability and the increase of oxidative levels were partially reversed. RNA-seq analysis showed that prolonged oxidation by Sin1 resulted in a simultaneous reduction of the expression level of endoplasmic reticulum (ER) genes that participate in proteostasis. By comparing the differential gene expression profile of Sin1 treated cells to cells incubated with ladostigil before being exposed to Sin1, we observed an over-expression of Clk1 (Cdc2-like kinase 1) which was implicated in psychophysiological stress in mice and Alzheimer’s disease. Ladostigil also suppressed the expression of Ccpg1 (Cell cycle progression 1) and Synj1 (Synaptojanin 1) that are involved in ER-autophagy and endocytic pathways. We postulate that ladostigil alleviated cell damage induced by oxidation. Therefore, under conditions of chronic stress that are observed in the aging brain, ladostigil may block oxidative stress processes and consequently reduce neurotoxicity.

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Vannelli, GB, F. Ensoli, R. Zonefrati, Y. Kubota, A. Arcangeli, A. Becchetti, G. Camici, T. Barni, CJ Thiele, and GC Balboni. "Neuroblast long-term cell cultures from human fetal olfactory epithelium respond to odors." Journal of Neuroscience 15, no. 6 (June 1, 1995): 4382–94. http://dx.doi.org/10.1523/jneurosci.15-06-04382.1995.

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Costine, Beth A., Symeon Missios, Sabrina R. Taylor, Declan McGuone, Colin M. Smith, Carter P. Dodge, Brent T. Harris, and Ann-Christine Duhaime. "The Subventricular Zone in the Immature Piglet Brain: Anatomy and Exodus of Neuroblasts into White Matter after Traumatic Brain Injury." Developmental Neuroscience 37, no. 2 (2015): 115–30. http://dx.doi.org/10.1159/000369091.

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Stimulation of postnatal neurogenesis in the subventricular zone (SVZ) and robust migration of neuroblasts to the lesion site in response to traumatic brain injury (TBI) is well established in rodent species; however, it is not yet known whether postnatal neurogenesis plays a role in repair after TBI in gyrencephalic species. Here we describe the anatomy of the SVZ in the piglet for the first time and initiate an investigation into the effect of TBI on the SVZ architecture and the number of neuroblasts in the white matter. Among all ages of immaturity examined the SVZ contained a dense mesh network of neurogenic precursor cells (doublecortin+) positioned directly adjacent to the ependymal cells (ventricular SVZ, Vsvz) and neuroblasts organized into chains that were distinct from the Vsvz (abventricular SVZ, Asvz). Though the architecture of the SVZ was similar among ages, the areas of Vsvz and Asvz neuroblast chains declined with age. At postnatal day (PND) 14 the white matter tracts have a tremendous number of individual neuroblasts. In our scaled cortical impact model, lesion size increased with age. Similarly, the response of the SVZ to injury was also age dependent. The younger age groups that sustained the proportionately smallest lesions had the largest SVZ areas, which further increased in response to injury. In piglets that were injured at 4 months of age and had the largest lesions, the SVZ did not increase in response to injury. Similar to humans, swine have abundant gyri and gyral white matter, providing a unique platform to study neuroblasts potentially migrating from the SVZ to the lesioned cortex along these white matter tracts. In piglets injured at PND 7, TBI did not increase the total number of neuroblasts in the white matter compared to uninjured piglets, but redistribution occurred with a greater number of neuroblasts in the white matter of the hemisphere ipsilateral to the injury compared to the contralateral hemisphere. At 7 days after injury, less than 1% of neuroblasts in the white matter were born in the 2 days following injury. These data show that the SVZ in the piglet shares many anatomical similarities with the SVZ in the human infant, and that TBI had only modest effects on the SVZ and the number of neuroblasts in the white matter. Piglets at an equivalent developmental stage to human infants were equipped with the largest SVZ and a tremendous number of neuroblasts in the white matter, which may be sufficient in lesion repair without the dramatic stimulation of neurogenic machinery. It has yet to be determined whether neurogenesis and migrating neuroblasts play a role in repair after TBI and/or whether an alteration of normal migration during active postnatal population of brain regions is beneficial in species with gyrencephalic brains.

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Erhardt, Nola M., Erica A. Fradinger, Laura A. Cervini, Jean E. Rivier, and Nancy M. Sherwood. "Early Expression of Pituitary Adenylate Cyclase-Activating Polypeptide and Activation of its Receptor in Chick Neuroblasts*." Endocrinology 142, no. 4 (April 1, 2001): 1616–25. http://dx.doi.org/10.1210/endo.142.4.8105.

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Abstract To investigate the involvement of pituitary adenylate cyclase- activating polypeptide (PACAP) and GH-releasing factor (GRF) during early chick brain development, we established neuroblast- enriched primary cell cultures derived from embryonic day 3.5 chick brain. We measured increases in cAMP generated by several species-specific forms of the peptides. Dose-dependent increases up to 5-fold of control values were measured in response to physiological concentrations of human/salmon, chicken, and tunicate PACAP27. Responses to PACAP38 were more variable, ranging from 5-fold for human PACAP38 to 4-fold for chicken PACAP38, to no significant response for salmon PACAP38, compared with control values. The responses to PACAP38 may reflect a greater difference in peptide structure compared with PACAP27 among species. Increases in cAMP generated by human, chicken, and salmon/carp GRF were not statistically significant, whereas increases in response to lower-range doses of tunicate GRF27-like peptide were significant, but small. We also used immunocytochemistry and Western blot to show synthesis of the PACAP38 peptide. RT-PCR was used to demonstrate that messenger RNAs for PACAP and GRF and a PACAP-specific receptor were present in the cells. This is a first report suggesting an autocrine/paracrine system for PACAP in early chick brain development, based on the presence of the ligand, messages for the ligand and receptor, and activation of the receptor in neuroblast-enriched cultures.

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Duan, Dah-Shuhn, Diana Farmer, Anthony A. Rayner, and Wolfgang Sadee. "Cytotoxicity of lymphokine-activated killer cells against human neuroblastoma cells: Modulation by neuroblast differentiation." Medical and Pediatric Oncology 18, no. 4 (1990): 339–44. http://dx.doi.org/10.1002/mpo.2950180418.

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Kragie, L., and D. Doyle. "Benzodiazepines inhibit temperature-dependent L-[125I]triiodothyronine accumulation into human liver, human neuroblast, and rat pituitary cell lines." Endocrinology 130, no. 3 (March 1992): 1211–16. http://dx.doi.org/10.1210/endo.130.3.1537286.

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Kragie, L. "Benzodiazepines inhibit temperature-dependent L-[125I]triiodothyronine accumulation into human liver, human neuroblast, and rat pituitary cell lines." Endocrinology 130, no. 3 (March 1, 1992): 1211–16. http://dx.doi.org/10.1210/en.130.3.1211.

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Zheng, Shanqing, Hilton Chiu, Jeffrey Boudreau, Tony Papanicolaou, William Bendena, and Ian Chin-Sang. "A functional study of all 40 Caenorhabditis elegans insulin-like peptides." Journal of Biological Chemistry 293, no. 43 (September 11, 2018): 16912–22. http://dx.doi.org/10.1074/jbc.ra118.004542.

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The human genome encodes 10 insulin-like genes, whereas the Caenorhabditis elegans genome remarkably encodes 40 insulin-like genes. Knockout strategies to determine the roles of all the insulin/insulin-like peptide ligands (INS) in C. elegans has been challenging due to functional redundancy. Here, we individually overexpressed each of the 40 ins genes pan-neuronally, and monitored multiple phenotypes including: L1 arrest life span, neuroblast divisions under L1 arrest, dauer formation, and fat accumulation, as readouts to characterize the functions of each INS in vivo. Of the 40 INS peptides, we found functions for 35 INS peptides and functionally categorized each as agonists, antagonists, or of pleiotropic function. In particular, we found that 9 of 16 agonistic INS peptides shortened L1 arrest life span and promoted neuroblast divisions during L1 arrest. Our study revealed that a subset of β-class INS peptides that contain a distinct F peptide sequence are agonists. Our work is the first to categorize the structures of INS peptides and relate these structures to the functions of all 40 INS peptides in vivo. Our findings will promote the study of insulin function on development, metabolism, and aging-related diseases.

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Zhu, Ziman, Peiling Huang, Ruifeng Sun, Xiaoling Li, Wenshan Li, and Weijun Gong. "A Novel Long-Noncoding RNA LncZFAS1 Prevents MPP+-Induced Neuroinflammation Through MIB1 Activation." Molecular Neurobiology 59, no. 2 (November 13, 2021): 778–99. http://dx.doi.org/10.1007/s12035-021-02619-z.

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AbstractParkinson’s disease remains one of the leading neurodegenerative diseases in developed countries. Despite well-defined symptomology and pathology, the complexity of Parkinson’s disease prevents a full understanding of its etiological mechanism. Mechanistically, α-synuclein misfolding and aggregation appear to be central for disease progression, but mitochondrial dysfunction, dysfunctional protein clearance and ubiquitin/proteasome systems, and neuroinflammation have also been associated with Parkinson’s disease. Particularly, neuroinflammation, which was initially thought to be a side effect of Parkinson’s disease pathogenesis, has now been recognized as driver of Parkinson’s disease exacerbation. Next-generation sequencing has been used to identify a plethora of long noncoding RNAs (lncRNA) with important transcriptional regulatory functions. Moreover, a myriad of lncRNAs are known to be regulators of inflammatory signaling and neurodegenerative diseases, including IL-1β secretion and Parkinson’s disease. Here, LncZFAS1 was identified as a regulator of inflammasome activation, and pyroptosis in human neuroblast SH-SY5Y cells following MPP+ treatment, a common in vitro Parkinson’s disease cell model. Mechanistically, TXNIP ubiquitination through MIB1 E3 ubiquitin ligase regulates NLRP3 inflammasome activation in neuroblasts. In contrast, MPP+ activates the NLPR3 inflammasome through miR590-3p upregulation and direct interference with MIB1-dependent TXNIP ubiquitination. LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p, exposing a novel research idea regarding the mechanism of Parkinson’s disease.

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Ben Othman, Sana, Nakako Katsuno, Akemi Kitayama, Makoto Fujimura, Kohji Kitaguchi, and Tomio Yabe. "White sesame seed water-soluble fraction enhances human neuroblast cell viability via an anti-apoptotic mechanism." Nutrition Research 36, no. 10 (October 2016): 1130–39. http://dx.doi.org/10.1016/j.nutres.2016.07.007.

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Savel'ev, S. V. "THE EARLY EMBRYONAL ANOMALIES OF HUMAN BRAIN." Annals of the Russian academy of medical sciences 67, no. 8 (August 11, 2012): 40–46. http://dx.doi.org/10.15690/vramn.v67i8.348.

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The mechanisms of early embryonic pathology of the brain in man and animals were studied. Analysis of the biomechanical properties of development of nervous tissue and embryonal experiments demonstrated that tangential neuroepithelial intention is the major source of positional information. Experimental changes in the neuroepithelial intention system resulted in various types of embryonal anomalies of the nervous system. Mechanical-dependent ion channels that have marked periods of sensitivity and determine the histogenetic direction of neuroblast cell differentiation were found to underline the mechanosensitivity of the neuroepithelium. Experimental findings were compared with unique autopsy data on early development of the human brain. Human embryos were examined from neurulation to month 6 of development. Different types of human embryonal brain anomalies were shown to occur with 3 types of neurulation disordes: 1) an open preneuropore is responsible for anomalies of the forebrain and etmoidal area; 2) arrested neurulation in the postneuropore leads to anomalies of the diencephalons, midbrain, and occipital region; 3) impaired neurulatuion in the caudal region is a cause of spinal cord anomalies. The above anomalies resulted from local compensatory responses of the neuroepithelium due to the lack of intentions that are characteristic of normal development of the neural tube.

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Ragusa, Marco, Alessandra Majorana, Barbara Banelli, Davide Barbagallo, Luisa Statello, Ida Casciano, Maria Rosa Guglielmino, et al. "MIR152, MIR200B, and MIR338, human positional and functional neuroblastoma candidates, are involved in neuroblast differentiation and apoptosis." Journal of Molecular Medicine 88, no. 10 (June 25, 2010): 1041–53. http://dx.doi.org/10.1007/s00109-010-0643-0.

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Luciani, Paola, Cristiana Deledda, Fabiana Rosati, Susanna Benvenuti, Ilaria Cellai, Francesca Dichiara, Matteo Morello, et al. "Seladin-1 Is a Fundamental Mediator of the Neuroprotective Effects of Estrogen in Human Neuroblast Long-Term Cell Cultures." Endocrinology 149, no. 9 (May 22, 2008): 4256–66. http://dx.doi.org/10.1210/en.2007-1795.

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Estrogen exerts neuroprotective effects and reduces β-amyloid accumulation in models of Alzheimer’s disease (AD). A few years ago, a new neuroprotective gene, i.e. seladin-1 (for selective AD indicator-1), was identified and found to be down-regulated in AD vulnerable brain regions. Seladin-1 inhibits the activation of caspase-3, a key modulator of apoptosis. In addition, it has been demonstrated that the seladin-1 gene encodes 3β-hydroxysterol Δ24-reductase, which catalyzes the synthesis of cholesterol from desmosterol. We have demonstrated previously that in fetal neuroepithelial cells, 17β-estradiol (17βE2), raloxifene, and tamoxifen exert neuroprotective effects and increase the expression of seladin-1. The aim of the present study was to elucidate whether seladin-1 is directly involved in estrogen-mediated neuroprotection. Using the small interfering RNA methodology, significantly reduced levels of seladin-1 mRNA and protein were obtained in fetal neuroepithelial cells. Seladin-1 silencing determined the loss of the protective effect of 17βE2 against β-amyloid and oxidative stress toxicity and caspase-3 activation. A computer-assisted analysis revealed the presence of half-palindromic estrogen responsive elements upstream from the coding region of the seladin-1 gene. A 1490-bp region was cloned in a luciferase reporter vector, which was transiently cotransfected with the estrogen receptor α in Chinese hamster ovarian cells. The exposure to 17βE2, raloxifene, tamoxifen, and the soy isoflavones genistein and zearalenone increased luciferase activity, thus suggesting a functional role for the half-estrogen responsive elements of the seladin-1 gene. Our data provide for the first time a direct demonstration that seladin-1 may be considered a fundamental mediator of the neuroprotective effects of estrogen.

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de Faria, Flavia W., Carolin Walter, Marta Interlandi, Viktoria Melcher, Nicole Riedel, Monika Graf, Natalia Moreno, et al. "ETMR-05. Single-cell transcriptomics of ETMR reveals developmental cellular programs and tumor-pericyte communications in the microenvironment." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i50. http://dx.doi.org/10.1093/neuonc/noac079.183.

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Abstract BACKGROUND: Embryonal tumors with multilayered rosettes (ETMR) are pediatric brain tumors bearing a grim prognosis, despite intensive multimodal therapeutic approaches. Insights into cellular heterogeneity and cellular communication of tumor cells with cells of the tumor microenvironment (TME), by applying single-cell (sc) techniques, potentially identify mechanisms of therapy resistance and target-directed treatment approaches. MATERIAL AND METHODS: To explore ETMR cell diversity, we used single-cell RNA sequencing (scRNA-seq) in human (n=2) and murine ETMR (transgenic mode; n=4) samples, spatial transcriptomics, 2D and 3D cultures (including co-cultures with TME cells), multiplex immunohistochemistry and drug screens. RESULTS: ETMR microenvironment is composed of tumor and non-tumor cell types. The ETMR malignant compartment harbour cells representing distinct transcriptional metaprograms, (NSC-like, NProg-like and Neuroblast-like), mirroring embryonic neurogenic cell states and fuelled by neurogenic pathways (WNT, SHH, Hippo). The ETMR TME is composed of oligodendrocyte and neuronal progenitor cells, neuroblasts, microglia, and pericytes. Tumor-specific ligand-receptor interaction analysis showed enrichment of intercellular communication between NProg-like ETMR cells and pericytes (PC). Functional network analyses reveal ETMR-PC interactions related to stem-cell signalling and extracellular matrix (ECM) organization, involving factors of the WNT, BMP, and CxCl12 networks. Results from ETMR-PC co-culture and spatial transcriptomics pointed to a pivotal role of pericytes in keeping ETMR in a germinal neurogenic state, enriched in stem-cell signalling. Drug screening considering cellular heterogeneity and cellular communication suggested novel therapeutic approaches. CONCLUSION: ETMR demonstrated diversity in the microenvironment, with enrichment of cell-cell communications with pericytes, supporting stem-cell signalling and interfering in the organization of the tumor extracellular matrix. Targeting ETMR-PC interactions might bring new opportunities for target-directed therapy.

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Ben Othman, Sana, Nakako Katsuno, Akemi Kitayama, Makoto Fujimura, Kohji Kitaguchi, and Tomio Yabe. "Water-soluble fractions from defatted sesame seeds protect human neuroblast cells against peroxyl radicals and hydrogen peroxide-induced oxidative stress." Free Radical Research 50, no. 9 (July 19, 2016): 949–58. http://dx.doi.org/10.1080/10715762.2016.1207248.

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Nag, T. C., and S. Wadhwa. "Expression of GABA in the fetal, postnatal, and adult human retinas: An immunohistochemical study." Visual Neuroscience 14, no. 3 (May 1997): 425–32. http://dx.doi.org/10.1017/s0952523800012104.

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AbstractThe expression of GABA in the human fetal (12–25 weeks of gestation), postnatal (five-month-old), and adult (35-year-old) retinas was investigated by immunohistochemistry. GABA expression was seen as early as 12 weeks in the undifferentiated cells of the inner neuroblast zone; a few optic nerve fiber layer axons were clearly labeled, suggesting that some of the stained cell bodies were prospective ganglion cells, others could be displaced amacrine cells. From 16–17 to 24–25 weeks, intense labeling was found in the amacrine, displaced amacrine, and some ganglion cells. During this time period, horizontal cells (identified by calbindin immunohistochemistry), undergoing migration (periphery) and differentiation (center), expressed GABA prominently. In the postnatal retina, some horizontal cells were moderately labeled, but very weakly in a few cells, in the adult. The Müller cells developed immunoreactivity first weakly at 12 weeks and then moderately from 16–17 weeks onward. The staining was also evident in the postnatal and adult retinas, showing labeled processes of these glial cells. Virtually no axons in the adult optic nerve and nerve fiber layer were stained; the staining was restricted to a few, large ganglion cells and displaced amacrine cells. Some amacrines were also labeled. The possibility that GABA might play a role in horizontal cell differentiation and maturation is highlighted. Other evidences suggest that GABA might play a role in metabolism during retinal development.

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Savare, Jean, Nathalie Bonneaud, and Franck Girard. "SUMO Represses Transcriptional Activity of the Drosophila SoxNeuro and Human Sox3 Central Nervous System–specific Transcription Factors." Molecular Biology of the Cell 16, no. 6 (June 2005): 2660–69. http://dx.doi.org/10.1091/mbc.e04-12-1062.

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Sry high mobility group (HMG) box (Sox) transcription factors are involved in the development of central nervous system (CNS) in all metazoans. Little is known on the molecular mechanisms that regulate their transcriptional activity. Covalent posttranslational modification by small ubiquitin-like modifier (SUMO) regulates several nuclear events, including the transcriptional activity of transcription factors. Here, we demonstrate that SoxNeuro, an HMG box-containing transcription factor involved in neuroblast formation in Drosophila, is a substrate for SUMO modification. SUMOylation assays in HeLa cells and Drosophila S2 cells reveal that lysine 439 is the major SUMO acceptor site. The sequence in SoxNeuro targeted for SUMOylation, IKSE, is part of a small inhibitory domain, able to repress in cis the activity of two adjacent transcriptional activation domains. Our data show that SUMO modification represses SoxNeuro transcriptional activity in transfected cells. Overexpression in Drosophila embryos of a SoxN form that cannot be targeted for SUMOylation strongly impairs the development of the CNS, suggesting that SUMO modification of SoxN is crucial for regulating its activity in vivo. Finally, we present evidence that SUMO modification of group B1 Sox factors was conserved during evolution, because Sox3, the human counterpart of SoxN, is also negatively regulated through SUMO modification.

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Sreeja, M. T., P. Vatsalaswamy, and A. S. Leo Rathinaraj. "Morphometric study of the neurons in human hypoglossal nerve nucleus during early gestation." Anatomy Journal of Africa 7, no. 2 (August 28, 2018): 1274–80. http://dx.doi.org/10.4314/aja.v7i2.176681.

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Hypoglossal nerve, XII cranial nerve is responsible for the motor innervation of the tongue muscles, which assists in various motor activities such as chewing, swallowing, vocalization. Thus, weakness of this nerve will lead to weakness and deviation of the tongue to one side. Clinically besides these functions it is also responsible for the most important function such as modulation of respiration and drinking behavior. Thus, a detailed study about the cell dynamics, which involves the development of neurons in the hypoglossal nerve nucleus becomes essential. 12 foetuses [Gestational age 10 – 24 weeks] were included in the study. They were divided into 4 groups based on their gestational age and CRL measurements. Hypoglossal nucleus extends throughout the length of medulla oblongata in the para-median plane. Tissues were collected from hind brain section and section of medulla. The tissues will be processed by routine histological procedure were stained with hematoxylin & eosin and also with Holmer’s Silver nitrate to study the histological details. Morphometric study covered the cell dimensions and volumes of hypoglossal neurons and its nucleus. From these data, coefficients were drawn to identify the proportion of growth between cell and nuclear volume. Morphometric analysis of hypoglossal nerve neurons in human from 10th to 24th gestational week concludes that the primitive migratory cells seen in the initial period and later it will become round neuroblast. In the initial 16 weeks nucleus occupied the entire volume of the cell.Keywords: Hypoglossal nerve nucleus, Deglutition, Mastication, Morphometry, Histogenesis

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Ramachandran, Haribaskar, Soraia Martins, Zacharias Kontarakis, Jean Krutmann, and Andrea Rossi. "Fast but not furious: a streamlined selection method for genome-edited cells." Life Science Alliance 4, no. 6 (April 26, 2021): e202101051. http://dx.doi.org/10.26508/lsa.202101051.

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In the last decade, transcription activator-like effector nucleases and CRISPR-based genome engineering have revolutionized our approach to biology. Because of their high efficiency and ease of use, the development of custom knock-out and knock-in animal or cell models is now within reach for almost every laboratory. Nonetheless, the generation of genetically modified cells often requires a selection step, usually achieved by antibiotics or fluorescent markers. The choice of the selection marker is based on the available laboratory resources, such as cell types, and parameters such as time and cost should also be taken into consideration. Here, we present a new and fast strategy called magnetic-activated genome-edited cell sorting, to select genetically modified cells based on the ability to magnetically sort surface antigens (i.e., tCD19) present in Cas9-positive cells. By using magnetic-activated genome-edited cell sorting, we successfully generated and isolated genetically modified human-induced pluripotent stem cells, primary human fibroblasts, SH-SY5Y neuroblast-like cells, HaCaT and HEK 293T cells. Our strategy expands the genome editing toolbox by offering a fast, cheap, and an easy to use alternative to the available selection methods.

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Ponzoni, M., and P. Cornaglia-Ferraris. "Interferon-γ-stimulated and GTP-binding-proteins-mediated phospholipase A2 activation in human neuroblasts." Biochemical Journal 294, no. 3 (September 15, 1993): 893–98. http://dx.doi.org/10.1042/bj2940893.

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Interferon-gamma (IFN-gamma) is a potent growth-inhibitory cytokine also endowed with differentiating activity on neural cells. Binding of IFN-gamma to its high-affinity receptor induces a rapid and transient activation of phospholipase A2 (PLA2). The mechanism coupling the IFN-gamma receptor (IFN-gamma-R) to PLA2 activation is not clearly defined, and no information is available on this mechanism in neuroblast cells. We have tested the hypothesis that GTP-binding proteins (G-proteins) may couple the IFN-gamma-R to PLA2 in the human neuroblastoma (NB) cell line LAN-5. Incubation of NB cells with IFN-gamma resulted in a rapid increase in [3H]arachidonic acid (AA) release, and this effect was blocked by pretreatment with anti-IFN-gamma antibodies. IFN-gamma-stimulated AA release was still observed in permeabilized cells that were blocked by pretreatment with anti-IFN-gamma-R antibodies. Exposure of permeabilized LAN-5 cells to guanosine 5′-[gamma-thio]triphosphate (GTP[S]), a non-hydrolysable GTP analogue, induced a dose-dependent release of [3H]AA. A non-specific nucleotide effect was excluded, since similar stimulatory effects on AA mobilization were not observed by GTP, ATP, CTP, ADP and GDP. IFN-gamma-stimulated AA release was completely blocked by the guanine nucleotide analogue that inhibits G-protein function, guanosine 5′-[beta-thio]diphosphate (GDP[S]). A role for G-proteins in IFN-gamma-R coupling to PLA2 was further supported by the inhibition of IFN-gamma-induced [3H]AA release by treatment of permeabilized cells with pertussis toxin and with the antiserum against the common alpha-subunits of G-proteins. To determine a possible contribution to AA mobilization by the phospholipase C and diacyglycerol lipase pathway or by protein kinase C activation, the effects of neomycin, a phospholipase C inhibitor, and PMA (phorbol 12-myristate 13-acetate), a direct activator of protein kinase C, were investigated. Neither neomycin nor PMA affected either basal or IFN-gamma-stimulated AA release. Ca2+ concentration, which has been shown to regulate the activity of some PLA2s, does not appear to play an important role in the regulation of the IFN-gamma-stimulated PLA2 activity, since incubating permeabilized cells in different concentrations of Ca2+ induced AA release without affecting the IFN-gamma response. Altogether, these findings suggest the existence of IFN-gamma-R, which couples a Ca(2+)-independent PLA2 activation via pertussis-toxin-sensitive G-proteins.

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Kakimolo, T., Y. Imai, N. Funamizu, T. Takakuwa, and M. Kunimoto. "Toxicity assessment of the extract of compost as a final product from Bio-Toilet." Water Science and Technology 54, no. 11-12 (December 1, 2006): 421–28. http://dx.doi.org/10.2166/wst.2006.922.

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Bio-Toilet is the name of a dry closet or composting toilet using sawdust as an artificial soil matrix for bioconversion of human excrement into compost. Since feces and urine contain several chemicals such as pharmaceutical residues and endocrine disruptors and they may still remain in compost after biological reaction in the Bio-Toilet, it is required to examine the possibility of soil and/or groundwater pollution by applying compost to a soil system in farmland. In this study, toxicity of Bio-Toilet compost was evaluated by measuring the viability of human neuroblast (NB-1). The bio-assay was applied to the water extract of compost from the Bio-Toilets which are in practical use in Japan. The assay results showed that (1) the extract of feces showed no toxicity, and the extracts of unused sawdust had no or low level toxicity and (2) the extracts of composts had heavier toxicity than unused sawdust. These results implied that some chemicals that have toxicity were generated by biological reactions or accumulated in toilet system. The bio-assay results with fractionated organic matter by its molecular weight showed that the small molecular weight fraction had stronger toxicity than other fractions. The effect of inorganic matter on toxicity was examined by comparing the dose-response relationship of the extracts of compost with positive control with 1M of sodium chloride solution. The comparison showed that sodium concentration in the extract was too low to develop the toxicity and the effect of inorganic matter could be neglected in this study.

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Giannini, S., S. Benvenuti, P. Luciani, C. Manuelli, I. Cellai, C. Deledda, A. Pezzatini, et al. "Intermittent high glucose concentrations reduce neuronal precursor survival by altering the IGF system: the involvement of the neuroprotective factor DHCR24 (Seladin-1)." Journal of Endocrinology 198, no. 3 (July 8, 2008): 523–32. http://dx.doi.org/10.1677/joe-07-0613.

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The exposure of neurons to high glucose concentrations is considered a determinant of diabetic neuropathy, whereas members of the IGF system are neurotropic factors. Here, we investigated the effects of constant and intermittent high glucose concentrations on IGF1 and IGF-binding proteins (IGFBPs) in human neuroblast long-term cell cultures fetal neuroepithelial cells (FNC). These cells express the IGF1 receptor, and express and release in the culture medium IGFBP2, IGFBP4, and IGF1. The release of IGF1 was significantly increased by 17β-estradiol (10 nM). IGF1 (100 nM) treatment determined a significant increase of IGFBP2 and a decrease of IGFBP4 release. In addition, IGF1 (1–100 nM) stimulated FNC cell proliferation in a dose-dependent manner. We hypothesized that this effect may be, at least partially, due to IGF1-induced up-regulation of the expression of the Alzheimer's disease related gene SELADIN-1 (now known as DHCR24 ), which acts as a pro-survival factor for neuronal cells. Conversely, the exposure to intermittent (20/10 mM), but not stable (20 mM), high glucose concentrations decreased the release of IGF1 and IGFBP2 in the culture medium and inhibited FNC growth by inducing apoptosis. The latter was prevented by the addition of IGF1 to the culture medium. Furthermore, high glucose concentrations reduced the expression of DHCR24. In conclusion, our results indicate for the first time that intermittent high glucose concentrations, similar to those observed in poorly controlled diabetic patients, may contribute to the development of diabetic neuropathy by interfering with the tropic effects exerted by the IGF system, and suggest the involvement of the neuroprotective factor DHCR24.

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Ho, Manh Tin, Jiongming Lu, Paula Vazquez-Pianzola, and Beat Suter. "α-Phenylalanyl tRNA synthetase competes with Notch signaling through its N-terminal domain." PLOS Genetics 18, no. 4 (April 29, 2022): e1010185. http://dx.doi.org/10.1371/journal.pgen.1010185.

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The alpha subunit of the cytoplasmic Phenylalanyl tRNA synthetase (α-PheRS, FARSA in humans) displays cell growth and proliferation activities and its elevated levels can induce cell fate changes and tumor-like phenotypes that are neither dependent on the canonical function of charging tRNAPhe with phenylalanine nor on stimulating general translation. In intestinal stem cells of Drosophila midguts, α-PheRS levels are naturally slightly elevated and human FARSA mRNA levels are elevated in multiple cancers. In the Drosophila midgut model, elevated α-PheRS levels caused the accumulation of many additional proliferating cells resembling intestinal stem cells (ISCs) and enteroblasts (EBs). This phenotype partially resembles the tumor-like phenotype described as Notch RNAi phenotype for the same cells. Genetic interactions between α-PheRS and Notch suggest that their activities neutralize each other and that elevated α-PheRS levels attenuate Notch signaling when Notch induces differentiation into enterocytes, type II neuroblast stem cell proliferation, or transcription of a Notch reporter. These non-canonical functions all map to the N-terminal part of α-PheRS which accumulates naturally in the intestine. This truncated version of α-PheRS (α-S) also localizes to nuclei and displays weak sequence similarity to the Notch intracellular domain (NICD), suggesting that α-S might compete with the NICD for binding to a common target. Supporting this hypothesis, the tryptophan (W) residue reported to be key for the interaction between the NICD and the Su(H) BTD domain is not only conserved in α-PheRS and α-S, but also essential for attenuating Notch signaling.

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Benvenuti, Susanna, Paola Luciani, Gabriella Barbara Vannelli, Stefania Gelmini, Elisa Franceschi, Mario Serio, and Alessandro Peri. "Estrogen and Selective Estrogen Receptor Modulators Exert Neuroprotective Effects and Stimulate the Expression ofSelective Alzheimer’s Disease Indicator-1, a Recently Discovered Antiapoptotic Gene, in Human Neuroblast Long-Term Cell Cultures." Journal of Clinical Endocrinology & Metabolism 90, no. 3 (March 2005): 1775–82. http://dx.doi.org/10.1210/jc.2004-0066.

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Hu, Youli, Subathra Poopalasundaram, Anthony Graham, and Pierre-Marc Bouloux. "GnRH Neuronal Migration and Olfactory Bulb Neurite Outgrowth Are Dependent on FGF Receptor 1 Signaling, Specifically via the PI3K p110α Isoform in Chick Embryo." Endocrinology 154, no. 1 (January 1, 2013): 388–99. http://dx.doi.org/10.1210/en.2012-1555.

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Fibroblast growth factor (FGF) signaling is essential for both olfactory bulb (OB) morphogenesis and the specification, migration, and maturation of the GnRH-secreting neurons. Disruption of FGF signaling contributes to Kallmann syndrome characterized by both anosmia and sexual immaturity. However, several unanswered questions remain as to which specific FGF receptor (FGFR)-1 signaling pathways are necessary for OB and GnRH neuronal development. Here, using pharmacological phosphatidylinositol 3-kinase (PI3K) isoform-specific inhibitors, we demonstrate a central role for the PI3K p110α isoform as a downstream effector of FGFR1 signaling for both GnRH neuronal migration and OB development. We show that signaling via the PI3K p110α isoform is required for GnRH neuronal migration in explant cultures of embryonic day (E) 4 chick olfactory placodes. We also show that in ovo administration of LY294002, a global PI3K inhibitor as well as an inhibitor to the PI3K p110α isoform into the olfactory placode of E3 chick embryo impairs GnRH neuronal migration toward the forebrain. In contrast, in ovo PI3K inhibitor treatment produced no obvious defects on primary olfactory sensory neuron axonal targeting and bundle formation. We also demonstrate that anosmin-1 and FGF2 induced neuronal migration of immortalized human embryonic GnRH neuroblast cells (FNC-B4-hTERT) is mediated by modulating FGFR1 signaling via the PI3K p110α isoform, specifically through phosphorylation of the PI3K downstream effectors, Akt and glycogen synthase kinase-3β. Finally, we show that neurite outgrowth and elongation of OB neurons in E10 chick OB explants are also dependent on the PI3K p110α isoform downstream of FGFR1. This study provides mechanistic insight into the etiology of Kallmann syndrome.

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de Faria, Flavia W., Marta Interlandi, Natalia Moreno, Monika Graf, Viktoria Melcher, Thomas K. Albert, and Kornelius Kerl. "ETMR-05. SINGLE-CELL RNA-SEQ OF ETMR REVEALS CELL PROGRAMS OF DEVELOPMENTAL HIERARCHY AND CELLULAR DIVERSITY IN THE TUMOR MICROENVIRONMENT." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii323. http://dx.doi.org/10.1093/neuonc/noaa222.209.

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Abstract Embryonal tumors with multilayered rosettes (ETMR) are deadly brain malignancies affecting young children. No standard treatment is available and the median survival is less than 12 months. Molecularly, the disease is characterized by the miRNA C19MC cluster amplification, with the expression of multiples miRNAs related to a stem cell program. The discoveries on the purely molecular mechanisms of the disease did not help to create a bridge for new treatment strategies so far and the cellular diversity of ETMR remains poorly understood. In this study, we used single-cell RNA sequencing of murine and human tumors to describe ETMR cellular heterogeneity. Our findings support that intra-tumoral heterogeneity is mainly characterized by 4 cellular programs defining a developmental hierarchy related to different metabolic states: 1) Early quiescent NSC-like cells supported by fatty-acid oxidation 2) Late NSC and NP-like proliferative cells fueled by glycolytic metabolism; 3) Post-mitotic neuroblast-like cells, relying on oxidative-phosphorylation; 4) NSC-like proliferative cells, with metabolic plasticity and capable of performing the three types of metabolism. Tumor-specific ligand-receptor interaction analysis revealed that ETMR exchange with microglia and vascular mural cells (MC) signals related to extracellular matrix (ECM) organization (Cxcl12-CxCr4), stem cell signaling (BMPs-BMP receptors), anti-apoptosis and survival (Ntf3-Ntrk), not seen in the control brain. In addition, the vascular MC showed a cancer-associated fibroblast (CAF) phenotype, with potential prognostic implications, as previously demonstrated for other tumors. This study provides new findings to build up a more robust understanding of ETMR biology and opens space for further studies in the field.

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de Trizio, Ignazio, Mariella Errede, Antonio d'Amati, Francesco Girolamo, and Daniela Virgintino. "Expression of P-gp in Glioblastoma: What we can Learn from Brain Development." Current Pharmaceutical Design 26, no. 13 (May 6, 2020): 1428–37. http://dx.doi.org/10.2174/1381612826666200318130625.

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P-Glycoprotein (P-gp) is a 170-kDa transmembrane glycoprotein that works as an efflux pump and confers multidrug resistance (MDR) in normal tissues and tumors, including nervous tissues and brain tumors. In the developing telencephalon, the endothelial expression of P-gp, and the subcellular localization of the transporter at the luminal endothelial cell (EC) plasma membrane are early hallmarks of blood-brain barrier (BBB) differentiation and suggest a functional BBB activity that may complement the placental barrier function and the expression of P-gp at the blood-placental interface. In early fetal ages, P-gp has also been immunolocalized on radial glia cells (RGCs), located in the proliferative ventricular zone (VZ) of the dorsal telencephalon and now considered to be neural progenitor cells (NPCs). RG-like NPCs have been found in many regions of the developing brain and have been suggested to give rise to neural stem cells (NSCs) of adult subventricular (SVZ) neurogenic niches. The P-gp immunosignal, associated with RG-like NPCs during cortical histogenesis, progressively decreases in parallel with the last waves of neuroblast migrations, while ‘outer’ RGCs and the deriving astrocytes do not stain for the efflux transporter. These data suggest that in human glioblastoma (GBM), P-gp expressed by ECs may be a negligible component of tumor MDR. Instead, tumor perivascular astrocytes may dedifferentiate and resume a progenitor-like P-gp activity, becoming MDR cells and contribute, together with perivascular P-gpexpressing glioma stem-like cells (GSCs), to the MDR profile of GBM vessels. In conclusion, the analysis of Pgp immunolocalization during brain development may contribute to identify the multiple cellular sources in the GBM vessels that may be involved in P-gp-mediated chemoresistance and can be responsible for GBM therapy failure and tumor recurrence.

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Funke, Sebastian, Vanessa M. Beutgen, Lea Bechter, Carsten Schmelter, Vanessa Zurawski, Natarajan Perumal, Norbert Pfeiffer, and Franz H. Grus. "An In-Depth View of the Porcine Trabecular Meshwork Proteome." International Journal of Molecular Sciences 20, no. 10 (May 22, 2019): 2526. http://dx.doi.org/10.3390/ijms20102526.

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The house swine (Sus scrofa domestica Linnaeus 1758) is an important model organism regarding the study of neurodegenerative diseases, especially ocular neuropathies such as glaucoma. This is due to the high comparability of the porcine and human eye regarding anatomy and molecular features. In the pathogenesis of glaucoma, the trabecular meshwork (TM) forms a key ocular component in terms of intraocular pressure (IOP) elevation. Thereby, functional TM abnormalities are correlated with distinct proteomic alterations. However, a detailed analysis of the TM proteome has not been realized so far. Since the porcine eye has high potential as a model system to study ocular diseases such as glaucoma, the present study focuses on the in-depth analysis of the porcine TM proteome. By use of a bottom-up (BU) mass spectrometric (MS) platform utilizing electrospray ionization liquid chromatography tandem MS (LC-ESI-MS/MS) considering database-dependent and peptide de novo sequencing, more than 3000 TM proteins were documented with high confidence (FDR < 1%). A distinct number of proteins with neuronal association were revealed. To the best to our knowledge, many of these protein species have not been reported for TM tissue before such as reelin, centlein and high abundant neuroblast differentiation-associated protein AHNAK (AHNAK). Thereby, AHNAK might play a superordinate role in the TM regarding proposed tissue involvement in barrier function. Also, a high number of secretory proteins could be identified. The generated TM proteomic landscape underlines a multifunctional character of the TM beyond representing a simple drainage system. Finally, the protein catalogue of the porcine TM provides an in-depth view of the TM molecular landscape and will serve as an important reference map in terms of glaucoma research utilizing porcine animal models, porcine TM tissues and/or cultured TM cells.

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Ensoli, Fabrizio, Aurelio Cafaro, Valeria Fiorelli, Barbara Vannelli, Barbara Ensoli, and Carol J. Thiele. "HIV-1 Infection of Primary Human Neuroblasts." Virology 210, no. 1 (June 1995): 221–25. http://dx.doi.org/10.1006/viro.1995.1336.

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Cornaglia-Ferraris, P., A. De Maria, C. Cirillo, A. Cara, and G. Alessandri. "Adhesion of Human Neuroblasts to HIV-1 tat." Pediatric Research 38, no. 5 (November 1995): 792–96. http://dx.doi.org/10.1203/00006450-199511000-00025.

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Blanc, Etienne, David Goldschneider, Sétha Douc-Rasy, Jean Bénard, and Gilda Raguénez. "Wnt-5a gene expression in malignant human neuroblasts." Cancer Letters 228, no. 1-2 (October 2005): 117–23. http://dx.doi.org/10.1016/j.canlet.2004.11.061.

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37

Gulisano, Massimo, Stefania Pacini, Tiziana Punzi, Gabriele Morucci, Sara Quagliata, Giovanni Delfino, Erica Sarchielli, Mirca Marini, and Gabriella B. Vannelli. "Cadmium modulates proliferation and differentiation of human neuroblasts." Journal of Neuroscience Research 87, no. 1 (January 2009): 228–37. http://dx.doi.org/10.1002/jnr.21830.

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Douc-Rasy, Sétha, Michel Barrois, Maria Echeynne, Mourad Kaghad, Etienne Blanc, Gilda Raguenez, David Goldschneider, et al. "ΔN-p73α Accumulates in Human Neuroblastic Tumors." American Journal of Pathology 160, no. 2 (February 2002): 631–39. http://dx.doi.org/10.1016/s0002-9440(10)64883-3.

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Baral, Sonu Shrestha, Molly E. Lieux, and Patrick J. DiMario. "Nucleolar stress in Drosophila neuroblasts, a model for human ribosomopathies." Biology Open 9, no. 4 (March 17, 2020): bio046565. http://dx.doi.org/10.1242/bio.046565.

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Ferrandis, Eric, and Jean Bénard. "Activation of the human mdr1 gene promoter in differentiated neuroblasts." International Journal of Cancer 54, no. 6 (July 30, 1993): 987–91. http://dx.doi.org/10.1002/ijc.2910540621.

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Cara, A., M. Pecorara, and P. Cornaglia-Ferraris. "Analysis of CD4 gene expression in human fetal brain and neuroblasts." Cellular and Molecular Neurobiology 12, no. 2 (April 1992): 131–41. http://dx.doi.org/10.1007/bf00713367.

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Strömberg, Ingrid, Erik Sundström, Per Almqvist, Marc Bygdeman, Maria Johansson, John Hudson, Craig van Horne, Paula Bickford, and Barry Hoffer. "Human and Rat Monoaminergic Neuroblasts Grafted to Rats with Unilateral Dopamine Depletions." Journal of Neural Transplantation and Plasticity 3, no. 4 (1992): 229–30. http://dx.doi.org/10.1155/np.1992.229.

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Curtis, M. A., M. Kam, U. Nannmark, M. F. Anderson, M. Z. Axell, C. Wikkelso, S. Holtas, et al. "Human Neuroblasts Migrate to the Olfactory Bulb via a Lateral Ventricular Extension." Science 315, no. 5816 (February 15, 2007): 1243–49. http://dx.doi.org/10.1126/science.1136281.

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Lovelace, Michael D., Ben J. Gu, Steven S. Eamegdool, Michael W. Weible, James S. Wiley, David G. Allen, and Tailoi Chan-Ling. "P2X7 Receptors Mediate Innate Phagocytosis by Human Neural Precursor Cells and Neuroblasts." STEM CELLS 33, no. 2 (January 22, 2015): 526–41. http://dx.doi.org/10.1002/stem.1864.

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van Strien, Miriam E., Simone A. van den Berge, and Elly M. Hol. "Migrating neuroblasts in the adult human brain: a stream reduced to a trickle." Cell Research 21, no. 11 (June 21, 2011): 1523–25. http://dx.doi.org/10.1038/cr.2011.101.

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Ponzoni, M., E. Lucarelli, M. V. Corrias, and P. Cornaglia-Ferraris. "Protein kinase C isoenzymes in human neuroblasts involvement of PKCε in cell differentiation." FEBS Letters 322, no. 2 (May 10, 1993): 120–24. http://dx.doi.org/10.1016/0014-5793(93)81550-j.

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Weickert, Cynthia Shannon, Maree J. Webster, Sarah M. Colvin, Mary M. Herman, Thomas M. Hyde, Daniel R. Weinberger, and Joel E. Kleinman. "Localization of epidermal growth factor receptors and putative neuroblasts in human subependymal zone." Journal of Comparative Neurology 423, no. 3 (2000): 359–72. http://dx.doi.org/10.1002/1096-9861(20000731)423:3<359::aid-cne1>3.0.co;2-0.

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Jara, Nery, Manuel Cifuentes, Fernando Martínez, Iván González-Chavarría, Katterine Salazar, Lucas Ferrada, and Francisco Nualart. "Vitamin C Deficiency Reduces Neurogenesis and Proliferation in the SVZ and Lateral Ventricle Extensions of the Young Guinea Pig Brain." Antioxidants 11, no. 10 (October 14, 2022): 2030. http://dx.doi.org/10.3390/antiox11102030.

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Although scurvy, the severe form of vitamin C deficiency, has been almost eradicated, the prevalence of subclinical vitamin C deficiency is much higher than previously estimated and its impact on human health might not be fully understood. Vitamin C is an essential molecule, especially in the central nervous system where it performs numerous, varied and critical functions, including modulation of neurogenesis and neuronal differentiation. Although it was originally considered to occur only in the embryonic brain, it is now widely accepted that neurogenesis also takes place in the adult brain. The subventricular zone (SVZ) is the neurogenic niche where the largest number of new neurons are born; however, the effect of vitamin C deficiency on neurogenesis in this key region of the adult brain is unknown. Therefore, through BrdU labeling, immunohistochemistry, confocal microscopy and transmission electron microscopy, we analyzed the proliferation and cellular composition of the SVZ and the lateral ventricle (LVE) of adult guinea pigs exposed to a vitamin-C-deficient diet for 14 and 21 days. We found that neuroblasts in the SVZ and LVE were progressively and significantly decreased as the days under vitamin C deficiency elapsed. The neuroblasts in the SVZ and LVE decreased by about 50% in animals with 21 days of deficiency; this was correlated with a reduction in BrdU positive cells in the SVZ and LVE. In addition, the reduction in neuroblasts was not restricted to a particular rostro–caudal area, but was observed throughout the LVE. We also found that vitamin C deficiency altered cellular morphology at the ultrastructural level, especially the cellular and nuclear morphology of ependymal cells of the LVE. Therefore, vitamin C is essential for the maintenance of the SVZ cell populations required for normal activity of the SVZ neurogenic niche in the adult guinea pig brain. Based on our results from the guinea pig brain, we postulate that vitamin C deficiency could also affect neurogenesis in the human brain.

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Meyer, Gundela. "From the lateral edge to the center of the cortex: The development of the human insula." Neuroforum 24, no. 4 (November 27, 2018): A151—A158. http://dx.doi.org/10.1515/nf-2018-a008.

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Abstract The human insula is a key node in a neuronal network which integrates interoceptive stimuli from the own body, and exteroceptive stimuli from the environment, and thus maintains the autonomic, emotional and socio-cognitive homeostasis of the body. In the last years, the insula has come into the focus of attention. Comparative anatomical studies showed that in many species the insula forms the lateral edge of the cortex. Very little is known about the prenatal development of the human insula, which is the first cortical region to mature. The origin of the pyramidal neurons for the insula is a small sector of the proliferating ventricular/subventricular zone at the cortico-striatal boundary (CSB). The CSB contains the radial glia cells, which are stem cells and give rise to a dense fascicle of radial glia processes. This fascicle traverses the external capsule and serves as a migration substrate for the neuroblasts on their way from the CSB into the insula. Around the 10/11th week of gestation, the lateral ventricle and its adjacent structures including the CSB bend in a C-shaped fashion. The insula now develops between a dorsal, fronto-parietal and a ventral, temporal CSB, which provide descending and ascending streams of neuroblasts, respectively, migrating along the radial glia fascicle. As a consequence of the ventricular rotation during ontogenesis, the human insula changes its initial position at the lateral edge of the cortex to its final central location, which reflects its integrative functions in brain activity.

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Sartelet, H., E. Haddad, T. Imbriglio, M. Arsenault, S. Ohta, S. Barrette, D. Sinnett, C. Laverdiere, L. Oligny, and G. Vassal. "Expression of CD133 and poor outcome in neuroblastoma associated with chemoresistance mediated by AKT pathway." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 10007. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.10007.

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10007 Background: Neuroblastoma is a frequent childhood cancer with very heterogeneous prognosis. Recent studies showed that CD133 expression is an independent prognostic marker for low survival in several cancers like medulloblastoma. The aim of our study is to determine the prognostic value of CD133 expression in a large population of neuroblastoma and to determine the chemoresistance of neuroblasts expressing CD133. Methods: 280 tumor samples of neuroblastoma were screened for CD133 expression. Patients had a median follow-up of 7.15 years. One hundred eighteen patients were under one year of age with a median age of 27 months. There were 67 stage 1, 46 stage 2, 43 stage 3, 99 stage 4, and 25 stage 4S. The association of CD133 expression with relapse and survival were determined through univariate and multivariate analysis. Sensitivity of purified CD133+ neuroblasts isolated from 2 human neuroblastoma cell lines (SKNSH and NB10) to doxorubicin, vincristine and cisplatin was evaluated in vitro, as single agents or in combination with LY294002, a AKT inhibitor. Results: CD133 was expressed in 95 of 280 tumors (33%). There was a significant association between CD133 expression and the following poor prognosis co-variates: age (p<0.0001), INSS stage (p<0.0001), MYCN amplification (p<0.0001). Patients with a CD133+ tumor had a three year event-free and overall survival of 43±5% and 51±5%, respectively, as compared to patients with a CD133- tumor with 88±2% (P<0.001) and 95±2% (p<0.001). In a multivariate model, CD133 expression was independently associated with a decreased overall survival (p = 0.003) in the entire cohort. In vitro purified CD133+ neuroblasts were significantly resistant to chemotherapy as compared to their CD133- cells counterpart, but not in presence of the AKT inhibitor. In vitro treatment of unsorted neuroblasts with the three anticancer drugs significantly enriched the CD133+ subpopulation but not in presence of the AKT inhibitor. CD133plus; significantly expressed higher levels of activated proteins in the AKT pathway than CD133−. Conclusions: CD133 is independently associated with a worse outcome in patents with neuroblastoma. This prognosis factor is associated with in vitro resistance to chemotherapy involving activation of the AKT pathway. No significant financial relationships to disclose.

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Journal articles on the topic 'Human neuroblast'

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