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Journal articles on the topic 'Neural precursor'

Author: Grafiati

Published: 25 June 2021

Last updated: 9 February 2022

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1

Jarman, A. P., M. Brand, L. Y. Jan, and Y. N. Jan. "The regulation and function of the helix-loop-helix gene, asense, in Drosophila neural precursors." Development 119, no. 1 (September 1, 1993): 19–29. http://dx.doi.org/10.1242/dev.119.1.19.

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asense is a member of the achaete-scute complex (AS-C) of helix-loop-helix genes involved in Drosophila neurogenesis. Unlike the other AS-C members, which are expressed in subsets of the ectodermal areas (proneural clusters) that give rise to neural precursors, asense is one of a number of genes that are specifically expressed in the neural precursors themselves (neural precursor genes). We have identified a mutant asense phenotype that may reflect this later expression pattern. As a step in understanding the determination of neural precursors from the proneural clusters, we have investigated the potential role of the AS-C products as direct transcriptional activators of neural precursor genes by analysing the regulation of asense. Using genomic rescues and asense-lacZ fusion genes, the neural precursor regulatory element has been identified. We show that this element contains binding sites for AS-C/daughterless heterodimers. Delection of these sites reduces the expression from the fusion gene, but significant expression is still achieved, pointing to the existence of other regulators of asense in addition to the AS-C. asense differs from the other AS-C members in its expression pattern, regulation, mutant phenotype and some DNA-binding properities.

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2

Urun, Fatma Rabia, and Adrian W. Moore. "Visualizing Cell Cycle Phase Organization and Control During Neural Lineage Elaboration." Cells 9, no. 9 (September 17, 2020): 2112. http://dx.doi.org/10.3390/cells9092112.

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In neural precursors, cell cycle regulators simultaneously control both progression through the cell cycle and the probability of a cell fate switch. Precursors act in lineages, where they transition through a series of cell types, each of which has a unique molecular identity and cellular behavior. Thus, investigating links between cell cycle and cell fate control requires simultaneous identification of precursor type and cell cycle phase, as well as an ability to read out additional regulatory factor expression or activity. We use a combined FUCCI-EdU labelling protocol to do this, and then apply it to the embryonic olfactory neural lineage, in which the spatial position of a cell correlates with its precursor identity. Using this integrated model, we find the CDKi p27KIP1 has different regulation relative to cell cycle phase in neural stem cells versus intermediate precursors. In addition, Hes1, which is the principle transcriptional driver of neural stem cell self-renewal, surprisingly does not regulate p27KIP1 in this cell type. Rather, Hes1 indirectly represses p27KIP1 levels in the intermediate precursor cells downstream in the lineage. Overall, the experimental model described here enables investigation of cell cycle and cell fate control linkage from a single precursor through to a lineage systems level.

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3

Henion, P. D., and J. A. Weston. "Timing and pattern of cell fate restrictions in the neural crest lineage." Development 124, no. 21 (November 1, 1997): 4351–59. http://dx.doi.org/10.1242/dev.124.21.4351.

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The trunk neural crest of vertebrate embryos is a transient collection of precursor cells present along the dorsal aspect of the neural tube. These cells migrate on two distinct pathways and give rise to specific derivatives in precise embryonic locations. One group of crest cells migrates early on a ventral pathway and generates neurons and glial cells. A later-dispersing group migrates laterally and gives rise to melanocytes in the skin. These observations raise the possibility that the appearance of distinct derivatives in different embryonic locations is a consequence of lineage restrictions specified before or soon after the onset of neural crest cell migration. To test this notion, we have assessed when and in what order distinct cell fates are specified during neural crest development. We determined the proportions of different types of precursor cells in cultured neural crest populations immediately after emergence from the neural tube and at intervals as development proceeds. We found that the initial neural crest population was a heterogeneous mixture of precursors almost half of which generated single-phenotype clones. Distinct neurogenic and melanogenic sublineages were also present in the outgrowth population almost immediately, but melanogenic precursors dispersed from the neural tube only after many neurogenic precursors had already done so. A discrete fate-restricted neuronal precursor population was distinguished before entirely separate fate-restricted melanocyte and glial precursor populations were present, and well before initial neuronal differentiation. Taken together, our results demonstrate that lineage-restricted subpopulations constitute a major portion of the initial neural crest population and that neural crest diversification occurs well before overt differentiation by the asynchronous restriction of distinct cell fates. Thus, the different morphogenetic and differentiative behavior of neural crest subsets in vivo may result from earlier cell fate-specification events that generate developmentally distinct subpopulations that respond differentially to environmental cues.

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4

Namihira, Masakazu, Jun Kohyama, Katsunori Semi, Tsukasa Sanosaka, Benjamin Deneen, Tetsuya Taga, and Kinichi Nakashima. "Committed Neuronal Precursors Confer Astrocytic Potential on Residual Neural Precursor Cells." Developmental Cell 16, no. 2 (February 2009): 245–55. http://dx.doi.org/10.1016/j.devcel.2008.12.014.

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5

Fike, John R., Radoslaw Rola, and Charles L. Limoli. "Radiation Response of Neural Precursor Cells." Neurosurgery Clinics of North America 18, no. 1 (January 2007): 115–27. http://dx.doi.org/10.1016/j.nec.2006.10.010.

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6

Gangemi, Rosaria M. R., Antonio Daga, Daniela Marubbi, Nadia Rosatto, Maria C. Capra, and Giorgio Corte. "Emx2 in adult neural precursor cells." Mechanisms of Development 109, no. 2 (December 2001): 323–29. http://dx.doi.org/10.1016/s0925-4773(01)00546-9.

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7

Monje, Michelle L., Shinichiro Mizumatsu, John R. Fike, and Theo D. Palmer. "Irradiation induces neural precursor-cell dysfunction." Nature Medicine 8, no. 9 (August 5, 2002): 955–62. http://dx.doi.org/10.1038/nm749.

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8

Nicolas, M., and B. A. Hassan. "Amyloid precursor protein and neural development." Development 141, no. 13 (June 24, 2014): 2543–48. http://dx.doi.org/10.1242/dev.108712.

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9

Pi, Haiwei, and Cheng-Ting Chien. "Getting the edge: neural precursor selection." Journal of Biomedical Science 14, no. 4 (March 15, 2007): 467–73. http://dx.doi.org/10.1007/s11373-007-9156-4.

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10

Soares, Juliana, Glauber R. de S. Araujo, Cintia Santana, Diana Matias, Vivaldo Moura-Neto, Marcos Farina, Susana Frases, et al. "Membrane Elastic Properties during Neural Precursor Cell Differentiation." Cells 9, no. 6 (May 26, 2020): 1323. http://dx.doi.org/10.3390/cells9061323.

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Neural precursor cells differentiate into several cell types that display distinct functions. However, little is known about how cell surface mechanics vary during the differentiation process. Here, by precisely measuring membrane tension and bending modulus, we map their variations and correlate them with changes in neural precursor cell morphology along their distinct differentiation fates. Both cells maintained in culture as neural precursors as well as those plated in neurobasal medium reveal a decrease in membrane tension over the first hours of culture followed by stabilization, with no change in bending modulus. During astrocyte differentiation, membrane tension initially decreases and then increases after 72 h, accompanied by consolidation of glial fibrillary acidic protein expression and striking actin reorganization, while bending modulus increases following observed alterations. For oligodendrocytes, the changes in membrane tension are less abrupt over the first hours, but their values subsequently decrease, correlating with a shift from oligodendrocyte marker O4 to myelin basic protein expressions and a remarkable actin reorganization, while bending modulus remains constant. Oligodendrocytes at later differentiation stages show membrane vesicles with similar membrane tension but higher bending modulus as compared to the cell surface. Altogether, our results display an entire spectrum of how membrane elastic properties are varying, thus contributing to a better understanding of neural differentiation from a mechanobiological perspective.

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11

Kalyani, Anjali J., and Mahendra S. Rao. "Cell lineage in the developing neural tube." Biochemistry and Cell Biology 76, no. 6 (December 1, 1998): 1051–68. http://dx.doi.org/10.1139/o98-105.

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Acquisition of cell type specific properties in the spinal cord is a process of sequential restriction in developmental potential. A multipotent stem cell of the nervous system, the neuroepithelial cell, generates central nervous system and peripheral nervous system derivatives via the generation of intermediate lineage restricted precursors that differ from each other and from neuroepithelial cells. Intermediate lineage restricted neuronal and glial precursors termed neuronal restricted precursors and glial restricted precursors, respectively, have been identified. Differentiation is influenced by extrinsic environmental signals that are stage and cell type specific. Analysis in multiple species illustrates similarities between chick, rat, mouse, and human cell differentiation. The utility of obtaining these precursor cell types for gene discovery, drug screening, and therapeutic applications is discussed.Key words: stem cells, oligodendrocytes, astrocytes, neurons, spinal cord.

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12

Li, Yi-Chen, Li-Kai Tsai, Jyh-Horng Wang, and Tai-Horng Young. "A neural stem/precursor cell monolayer for neural tissue engineering." Biomaterials 35, no. 4 (January 2014): 1192–204. http://dx.doi.org/10.1016/j.biomaterials.2013.10.066.

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13

Wehrle-Haller, B., and J. A. Weston. "Soluble and cell-bound forms of steel factor activity play distinct roles in melanocyte precursor dispersal and survival on the lateral neural crest migration pathway." Development 121, no. 3 (March 1, 1995): 731–42. http://dx.doi.org/10.1242/dev.121.3.731.

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Trunk neural crest cells segregate from the neuroepithelium and enter a ‘migration staging area’ lateral to the embryonic neural tube. After some crest cells in the migration staging area have begun to migrate on a medial pathway, a subpopulation of crest-derived cells remaining in the migration staging area expresses mRNAs for the receptor tyrosine kinase, c-kit, and tyrosinase-related protein-2, both of which are characteristic of melanocyte precursors. These putative melanocyte precursors are subsequently observed on the lateral crest migration pathway between the dermatome and overlying epithelium, and then dispersed in nascent dermal mesenchyme. Melanocyte precursors transiently require the c-kit ligand, Steel factor for survival. Although Steel factor mRNA is transiently expressed in the dorsal dermatome before the onset of trunk neural crest cell dispersal on the lateral pathway, it is no longer produced by dermatomal cells when melanocyte precursors have dispersed in the dermal mesenchyme. To assess the role of Steel factor in migration of melanocyte precursors on the lateral pathway, we analyzed melanocyte precursor dispersal and fate on the lateral pathway of two different Sl mutants, Sl, a null allele, and Sld, which lacks cell surface-associated Steel factor but produces a soluble form. No melanocyte precursors were detected in the dermatome of embryos homozygous for the Sl allele or in W mutants that lack functional c-kit. In contrast, in embryos homozygous for the Sld allele, melanocyte precursors appeared on the lateral pathway, but subsequently disappear from the dermis. These results suggest that soluble Steel factor is required for melanocyte precursor dispersal on the lateral pathway, or for their initial survival in the migration staging area. In contrast, membrane-bound Steel factor appears to promote melanocyte precursor survival in the dermis.

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14

Leong, Soo Yuen, and Ann M. Turnley. "Regulation of adult neural precursor cell migration." Neurochemistry International 59, no. 3 (September 2011): 382–93. http://dx.doi.org/10.1016/j.neuint.2010.12.024.

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15

Fainstein, Nina, Ilan Vaknin, Ofira Einstein, Philip Zisman, S. Z. Ben Sasson, Michal Baniyash, and Tamir Ben-Hur. "Neural precursor cells inhibit multiple inflammatory signals." Molecular and Cellular Neuroscience 39, no. 3 (October 2008): 335–41. http://dx.doi.org/10.1016/j.mcn.2008.07.007.

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16

Neville, Craig M., Albert Y. Huang, Jeffrey Y. Shyu, Evan Y. Snyder, Tessa A. Hadlock, and Cathryn A. Sundback. "Neural Precursor Cell Lines Promote Neurite Branching." International Journal of Neuroscience 119, no. 1 (January 2009): 15–39. http://dx.doi.org/10.1080/00207450802480218.

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17

Sacco, Raffaele, Laura Tamblyn, Nishani Rajakulendran, Fernando N. Bralha, Vincent Tropepe, and Rebecca R. Laposa. "Cockayne syndrome b maintains neural precursor function." DNA Repair 12, no. 2 (February 2013): 110–20. http://dx.doi.org/10.1016/j.dnarep.2012.11.004.

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18

Zhao, Jing, Chanel J. Taylor, Estella A. Newcombe, Mark D. Spanevello, Imogen O’Keeffe, Leanne T. Cooper, Dhanisha J. Jhaveri, Andrew W. Boyd, and Perry F. Bartlett. "EphA4 Regulates Hippocampal Neural Precursor Proliferation in the Adult Mouse Brain by d-Serine Modulation of N-Methyl-d-Aspartate Receptor Signaling." Cerebral Cortex 29, no. 10 (December 22, 2018): 4381–97. http://dx.doi.org/10.1093/cercor/bhy319.

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Abstract The hippocampal dentate gyrus (DG) is a major region of the adult rodent brain in which neurogenesis occurs throughout life. The EphA4 receptor, which regulates neurogenesis and boundary formation in the developing brain, is also expressed in the adult DG, but whether it regulates adult hippocampal neurogenesis is not known. Here, we show that, in the adult mouse brain, EphA4 inhibits hippocampal precursor cell proliferation but does not affect precursor differentiation or survival. Genetic deletion or pharmacological inhibition of EphA4 significantly increased hippocampal precursor proliferation in vivo and in vitro, by blocking EphA4 forward signaling. EphA4 was expressed by mature hippocampal DG neurons but not neural precursor cells, and an EphA4 antagonist, EphA4-Fc, did not activate clonal cultures of precursors until they were co-cultured with non-precursor cells, indicating an indirect effect of EphA4 on the regulation of precursor activity. Supplementation with d-serine blocked the increased precursor proliferation induced by EphA4 inhibition, whereas blocking the interaction between d-serine and N-methyl-d-aspartate receptors (NMDARs) promoted precursor activity, even at the clonal level. Collectively, these findings demonstrate that EphA4 indirectly regulates adult hippocampal precursor proliferation and thus plays a role in neurogenesis via d-serine-regulated NMDAR signaling.

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19

Nishida, H. "Induction of brain and sensory pigment cells in the analyzed by experiments with isolated blastomeres." Development 112, no. 2 (June 1, 1991): 389–95. http://dx.doi.org/10.1242/dev.112.2.389.

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Tadpole larvae of ascidians have a brain and two kinds cells within the brain. These neural tissues are neural plate and, as in vertebrates, neural induction of the nervous system. The brain and pigment cells are animal (a-line) blastomeres, and inductive interaction line) blastomeres is necessary for formation of neural cells. In order to investigate the characteristics of blastomeres were isolated from embryos of Halocynthia (late blastula) stage, and then their developmental first set of experiments, brain- and pigment-lineage neural induction, failed to develop three specific (epithelial morphology, secretion of larval tunic and specific antigen). These observations suggested a neural induction, indicative perhaps of a permissive embryogenesis. Next, in order to identify which type the inducer of the sensory pigment cells, various sets isolated from 110-cell embryos, in which the fates of restricted to a single type of tissue. The results precursor blastomeres, which are cells of the A-line, a-line cells to form pigment cells. In addition, cord precursors had been ablated, failed to form a brain structure. Therefore, it is probable that the sensory pigment cells are the spinal-cord precursor

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20

Shivraj Sohur, U., Jason G. Emsley, Bartley D. Mitchell, and Jeffrey D. Macklis. "Adult neurogenesis and cellular brain repair with neural progenitors, precursors and stem cells." Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1473 (July 31, 2006): 1477–97. http://dx.doi.org/10.1098/rstb.2006.1887.

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Recent work in neuroscience has shown that the adult central nervous system (CNS) contains neural progenitors, precursors and stem cells that are capable of generating new neurons, astrocytes and oligodendrocytes. While challenging the previous dogma that no new neurons are born in the adult mammalian CNS, these findings bring with them the future possibilities for development of novel neural repair strategies. The purpose of this review is to present the current knowledge about constitutively occurring adult mammalian neurogenesis, highlight the critical differences between ‘neurogenic’ and ‘non-neurogenic’ regions in the adult brain, and describe the cardinal features of two well-described neurogenic regions—the subventricular zone/olfactory bulb system and the dentate gyrus of the hippocampus. We also provide an overview of presently used models for studying neural precursors in vitro , mention some precursor transplantation models and emphasize that, in this rapidly growing field of neuroscience, one must be cautious with respect to a variety of methodological considerations for studying neural precursor cells both in vitro and in vivo . The possibility of repairing neural circuitry by manipulating neurogenesis is an intriguing one, and, therefore, we also review recent efforts to understand the conditions under which neurogenesis can be induced in non-neurogenic regions of the adult CNS. This work aims towards molecular and cellular manipulation of endogenous neural precursors in situ , without transplantation. We conclude this review with a discussion of what might be the function of newly generated neurons in the adult brain, and provide a summary of present thinking about the consequences of disturbed adult neurogenesis and the reaction of neurogenic regions to disease.

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21

D'Sa-Eipper, C., J. R. Leonard, G. Putcha, T. S. Zheng, R. A. Flavell, P. Rakic, K. Kuida, and K. A. Roth. "DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3." Development 128, no. 1 (January 1, 2001): 137–46. http://dx.doi.org/10.1242/dev.128.1.137.

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Programmed cell death (apoptosis) is critical for normal brain morphogenesis and may be triggered by neurotrophic factor deprivation or irreparable DNA damage. Members of the Bcl2 and caspase families regulate neuronal responsiveness to trophic factor withdrawal; however, their involvement in DNA damage-induced neuronal apoptosis is less clear. To define the molecular pathway regulating DNA damage-induced neural precursor cell apoptosis, we have examined the effects of drug and gamma-irradiation-induced DNA damage on telencephalic neural precursor cells derived from wild-type embryos and mice with targeted disruptions of apoptosis-associated genes. We found that DNA damage-induced neural precursor cell apoptosis, both in vitro and in vivo, was critically dependent on p53 and caspase 9, but neither Bax nor caspase 3 expression. Neural precursor cell apoptosis was also unaffected by targeted disruptions of Bclx and Bcl2, and unlike neurotrophic factor-deprivation-induced neuronal apoptosis, was not associated with a detectable loss of cytochrome c from mitochondria. The apoptotic pathway regulating DNA damage-induced neural precursor cell death is different from that required for normal brain morphogenesis, which involves both caspase 9 and caspase 3 but not p53, indicating that additional apoptotic stimuli regulate neural precursor cell numbers during telencephalic development.

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22

Beltz, Barbara S., Georg Brenneis, and Jeanne L. Benton. "Adult Neurogenesis: Lessons from Crayfish and the Elephant in the Room." Brain, Behavior and Evolution 87, no. 3 (2016): 146–55. http://dx.doi.org/10.1159/000447084.

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The 1st-generation neural precursors in the crustacean brain are functionally analogous to neural stem cells in mammals. Their slow cycling, migration of their progeny, and differentiation of their descendants into neurons over several weeks are features of the neural precursor lineage in crayfish that also characterize adult neurogenesis in mammals. However, the 1st-generation precursors in crayfish do not self-renew, contrasting with conventional wisdom that proposes the long-term self-renewal of adult neural stem cells. Nevertheless, the crayfish neurogenic niche, which contains a total of 200-300 cells, is never exhausted and neurons continue to be produced in the brain throughout the animal's life. The pool of neural precursors in the niche therefore cannot be a closed system, and must be replenished from an extrinsic source. Our in vitro and in vivo data show that cells originating in the innate immune system (but not other cell types) are attracted to and incorporated into the neurogenic niche, and that they express a niche-specific marker, glutamine synthetase. Further, labeled hemocytes that undergo adoptive transfer to recipient crayfish generate cells in neuronal clusters in the olfactory pathway of the adult brain. These hemocyte descendants express appropriate neurotransmitters and project to target areas typical of neurons in these regions. These studies indicate that under natural conditions, the immune system provides neural precursors supporting adult neurogenesis in the crayfish brain, challenging the canonical view that ectodermal tissues generating the embryonic nervous system are the sole source of neurons in the adult brain. However, these are not the first studies that directly implicate the immune system as a source of neural precursor cells. Several types of data in mammals, including adoptive transfers of bone marrow or stem cells as well as the presence of fetal microchimerism, suggest that there must be a population of cells that are able to access the brain and generate new neurons in these species.

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23

Jiang, Limin, Jingjun Zhang, Ping Xuan, and Quan Zou. "BP Neural Network Could Help Improve Pre-miRNA Identification in Various Species." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9565689.

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MicroRNAs (miRNAs) are a set of short (21–24 nt) noncoding RNAs that play significant regulatory roles in cells. In the past few years, research on miRNA-related problems has become a hot field of bioinformatics because of miRNAs’ essential biological function. miRNA-related bioinformatics analysis is beneficial in several aspects, including the functions of miRNAs and other genes, the regulatory network between miRNAs and their target mRNAs, and even biological evolution. Distinguishing miRNA precursors from other hairpin-like sequences is important and is an essential procedure in detecting novel microRNAs. In this study, we employed backpropagation (BP) neural network together with 98-dimensional novel features for microRNA precursor identification. Results show that the precision and recall of our method are 95.53% and 96.67%, respectively. Results further demonstrate that the total prediction accuracy of our method is nearly 13.17% greater than the state-of-the-art microRNA precursor prediction software tools.

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24

Vanderluit, Jacqueline L., Crystal A. Wylie, Kelly A. McClellan, Noel Ghanem, Andre Fortin, Steve Callaghan, Jason G. MacLaurin, David S. Park, and Ruth S. Slack. "The Retinoblastoma family member p107 regulates the rate of progenitor commitment to a neuronal fate." Journal of Cell Biology 178, no. 1 (June 25, 2007): 129–39. http://dx.doi.org/10.1083/jcb.200703176.

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The Retinoblastoma protein p107 regulates the neural precursor pool in both the developing and adult brain. As p107-deficient mice exhibit enhanced levels of Hes1, we questioned whether p107 regulates neural precursor self-renewal through the repression of Hes1. p107 represses transcription at the Hes1 promoter. Despite an expanded neural precursor population, p107-null mice exhibit a striking reduction in the number of cortical neurons. Hes1 deficiency rescues neurosphere numbers in p107-null embryos. We find that the loss of a single Hes1 allele in vivo restores the number of neural precursor cells at the ventricular zone. Neuronal birthdating analysis reveals a dramatic reduction in the rate of neurogenesis, demonstrating impairment in p107−/− progenitors to commit to a neuronal fate. The loss of a single Hes1 allele restores the number of newly generated neurons in p107-deficient brains. Together, we identify a novel function for p107 in promoting neural progenitor commitment to a neuronal fate.

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25

Brand, M., A. P. Jarman, L. Y. Jan, and Y. N. Jan. "asense is a Drosophila neural precursor gene and is capable of initiating sense organ formation." Development 119, no. 1 (September 1, 1993): 1–17. http://dx.doi.org/10.1242/dev.119.1.1.

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Neural precursor cells in Drosophila arise from the ectoderm in the embryo and from imaginal disc epithelia in the larva. In both cases, this process requires daughterless and the proneural genes achaete, scute and lethal-of-scute of the achaete-scute complex. These genes encode basic helix-loop-helix proteins, which are nuclear transcription factors, as does the asense gene of the achaete-scute complex. Our studies suggest that asense is a neural precursor gene, rather than a proneural gene. Unlike the proneural achaete-scute gene products, the asense RNA and protein are found in the neural precursor during its formation, but not in the proneural cluster of cells that gives rise to the neural precursor cell. Also, asense expression persists longer during neural precursor development than the proneural gene products; it is still expressed after the first division of the neural precursor. Moreover, asense is likely to be downstream of the proneural genes, because (1) asense expression is affected in proneural and neurogenic mutant backgrounds, (2) ectopic expression of asense protein with an intact DNA-binding domain bypasses the requirement for achaete and scute in the formation of imaginal sense organs. We further note that asense ectopic expression is capable of initiating the sense organ fate in cells that do not normally require the action of asense. Our studies therefore serve as a cautionary note for the inference of normal gene function based on the gain-of-function phenotype after ectopic expression.

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26

Hisatsune, Tatsuhiro, Naoko Yoshida, Tomohiro Kaji, Kiyoshi Yamada, Cheng-Wen Lien, Ronald D. G. McKay, and Shuichi Kaminogawa. "Differentiation of telencephalic neural stem/precursor cell lines." Neuroscience Research 31 (January 1998): S319. http://dx.doi.org/10.1016/s0168-0102(98)82448-6.

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27

Mayer-Proschel, Margot, Ying Liu, Haipeng Xue, Yuanyuan Wu, Melissa K. Carpenter, and Mahendra S. Rao. "Human neural precursor cells – an in vitro characterization." Clinical Neuroscience Research 2, no. 1-2 (May 2002): 58–69. http://dx.doi.org/10.1016/s1566-2772(02)00007-5.

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28

Ben-Hur, T., H. S. Keirstead, B. Rogister, M. Dubois-Dalcq, and W. F. Blakemore. "Remyelination by PSA-NCAM+ neural precursor cell spheres." Journal of Neuroimmunology 90, no. 1 (September 1998): 26. http://dx.doi.org/10.1016/s0165-5728(98)91336-4.

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29

Sabolek, Michael, Anna Herborg, Johannes Schwarz, and Alexander Storch. "Dexamethasone blocks astroglial differentiation from neural precursor cells." NeuroReport 17, no. 16 (November 2006): 1719–23. http://dx.doi.org/10.1097/01.wnr.0000236862.08834.50.

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30

Bacigaluppi, Marco, Giacomo Sferruzza, Erica Butti, Linda Ottoboni, and Gianvito Martino. "Endogenous neural precursor cells in health and disease." Brain Research 1730 (March 2020): 146619. http://dx.doi.org/10.1016/j.brainres.2019.146619.

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31

Qiu, Jianhua, Yasushi Takagi, Jun Harada, Neil Rodrigues, Michael A. Moskowitz, David T. Scadden, and Tao Cheng. "Regenerative Response in Ischemic Brain Restricted by p21cip1/waf1." Journal of Experimental Medicine 199, no. 7 (April 5, 2004): 937–45. http://dx.doi.org/10.1084/jem.20031385.

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Neural precursor cells from adults have exceptional proliferative and differentiative capability in vitro yet respond minimally to in vivo brain injury due to constraining mechanisms that are poorly defined. We assessed whether cell cycle inhibitors that restrict stem cell populations in other tissues may participate in limiting neural stem cell reactivity in vivo. The cyclin-dependent kinase inhibitor, p21cip1/waf1 (p21), maintains hematopoietic stem cell quiescence, and we evaluated its role in the regenerative response of neural tissue after ischemic injury using the mice deficient in p21. Although steady-state conditions revealed no increase in primitive cell proliferation in p21-null mice, a significantly larger fraction of quiescent neural precursors was activated in the hippocampus and subventricular zone after brain ischemia. The hippocampal precursors migrated and differentiated into a higher number of neurons after injury. Therefore, p21 is an intrinsic suppressor to neural regeneration after brain injury and may serve as a common molecular regulator restricting proliferation among stem cell pools from distinct tissue types.

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32

Fernandes, Karl J. L., Jean G. Toma, and Freda D. Miller. "Multipotent skin-derived precursors: adult neural crest-related precursors with therapeutic potential." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1489 (February 5, 2007): 185–98. http://dx.doi.org/10.1098/rstb.2006.2020.

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We previously made the surprising finding that cultures of multipotent precursors can be grown from the dermis of neonatal and adult mammalian skin. These skin-derived precursors (SKPs) display multi-lineage differentiation potential, producing both neural and mesodermal progeny in vitro , and are an apparently novel precursor cell type that is distinct from other known precursors within the skin. In this review, we begin by placing these findings within the context of the rapidly evolving stem cell field. We then describe our recent efforts focused on understanding the developmental biology of SKPs, discussing the idea that SKPs are neural crest-related precursors that (i) migrate into the skin during embryogenesis, (ii) persist within a specific dermal niche, and (iii) play a key role in the normal physiology, and potentially pathology, of the skin. We conclude by highlighting some of the therapeutic implications and unresolved questions raised by these studies.

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33

Yuan, Xiaoyang, Jing Wang, and Hing Chan. "Sub-Nanomolar Methylmercury Exposure Promotes Premature Differentiation of Murine Embryonic Neural Precursor at the Expense of Their Proliferation." Toxics 6, no. 4 (October 10, 2018): 61. http://dx.doi.org/10.3390/toxics6040061.

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Methylmercury (MeHg) is a ubiquitous environmental pollutant that is known to be neurotoxic, particularly during fetal development. However, the mechanisms responsible for MeHg-induced changes in adult neuronal function, when their exposure occurred primarily during fetal development, are not yet understood. We hypothesized that fetal MeHg exposure could affect neural precursor development leading to long-term neurotoxic effects. Primary cortical precursor cultures obtained from embryonic day 12 were exposed to 0 nM, 0.25 nM, 0.5 nM, 2.5 nM, and 5 nM MeHg for 48 or 72 h. Total Hg accumulated in the harvested cells in a dose-dependent manner. Not all of the concentrations tested in the study affected cell viability. Intriguingly, we observed that cortical precursor exposed to 0.25 nM MeHg showed increased neuronal differentiation, while its proliferation was inhibited. Reduced neuronal differentiation, however, was observed in the higher dose groups. Our results suggest that sub-nanomolar MeHg exposure may deplete the pool of neural precursors by increasing premature neuronal differentiation, which can lead to long-term neurological effects in adulthood as opposed to the higher MeHg doses that cause more immediate toxicity during infant development.

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Wetts, Richard, and Scott E. Fraser. "Microinjection of fluorescent tracers to study neural cell lineages." Development 113, Supplement_2 (April 1, 1991): 1–8. http://dx.doi.org/10.1242/dev.113.supplement_2.1.

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The examination of cell lineages is an important step towards understanding the developmental events that specify the various cell types in the organism. The mechanisms that control which cell types are formed, their locations, and their numbers remain unknown. Analyses of cell lineage in the frog neural retina have revealed that individual precursors are multipotent and are capable of producing almost any combination of cell types. In addition to giving rise to a wide range of phenotypes, the precursors can give rise to a wide range of clone sizes. Cell lineage studies in other systems indicate that some precursors are multipotent, like those in the retina, while others appear to produce a more restricted range of descendants, perhaps even a single phenotype. These differences in the developmental potential of precursor cells suggest that the nervous system uses several strategies for producing its many cell types. Investigation of these strategies, at the cellular and molecular level, requires more than a description of the normal cell lineages. We are now exploiting the frog neural retina to perform the experimental manipulations needed to elucidate these strategies.

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Murphy, M., K. Reid, M. Ford, J. B. Furness, and P. F. Bartlett. "FGF2 regulates proliferation of neural crest cells, with subsequent neuronal differentiation regulated by LIF or related factors." Development 120, no. 12 (December 1, 1994): 3519–28. http://dx.doi.org/10.1242/dev.120.12.3519.

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Two of the key early events in the development of the peripheral nervous system are the proliferation of neural crest precursor cells and their subsequent differentiation into different neural cell types. We present evidence that members of the fibroblast growth factor family, (FGF1 or FGF2) act directly on the neural crest cells in vitro to stimulate proliferation in the presence of serum. These findings correlate with in situ hybridisation analysis, which shows FGF2 mRNA is expressed in cells both in the neural tube and within newly formed sensory ganglia (dorsal root ganglia, DRG) at embryonic day 10 in the mouse, when neural crest precursors are proliferating within the DRG. This data infers an autocrine/paracrine loop for FGF regulation of proliferation. Evidence supporting this notion is provided by the finding that part of the endogenous proliferative activity in the NC cultures is related to FGF. It was also found, in early neural crest cultures, that exogenous FGF completely inhibited neuronal differentiation, probably as a direct consequence of its mitogenic activity. In order to stimulate neuronal differentiation significantly, it was necessary to remove the FGF and replace it with leukemia inhibitory factor (LIF) or related factors. Under these conditions, 50% of the cells differentiated into neurons, which developed a sensory neuron morphology and were immunoreactive for the sensory markers CGRP and substance P. These data support a model of neural crest development, whereby multipotential neural crest precursor cells are stimulated to divide by FGF and subsequent development into sensory neurons is regulated by LIF or other cytokines with a similar signalling mechanism.

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Han, Youngmin, and Kyoung-Tae Kim. "Neural Growth Factor Stimulates Proliferation of Spinal Cord Derived-Neural Precursor/Stem Cells." Journal of Korean Neurosurgical Society 59, no. 5 (2016): 437. http://dx.doi.org/10.3340/jkns.2016.59.5.437.

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Tomooka, Y., H. Kitani, N. Jing, M. Matsushima, and T. Sakakura. "Reconstruction of neural tube-like structures in vitro from primary neural precursor cells." Proceedings of the National Academy of Sciences 90, no. 20 (October 15, 1993): 9683–87. http://dx.doi.org/10.1073/pnas.90.20.9683.

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Gilbert, Emily, Jessica Livingston, Monoleena Khan, Harini Kandavel, Tarlan Kehtari, and Cindi Morshead. "Activating Resident Neural Precursor Cells in the Spinal Cord to Promote Neural Repair." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.05449.

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Van Raay, Terence, Yu-Ker Wang, Michael Stark, Jennifer Rasmussen, Uta Francke, Monica Vetter, and Mahendra Rao. "frizzled 9 is expressed in neural precursor cells in the developing neural tube." Development Genes and Evolution 211, no. 8-9 (September 1, 2001): 453–57. http://dx.doi.org/10.1007/s004270100174.

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Dugani, Sagar, Annie Paquin, Masashi Fujitani, David R. Kaplan, and Freda D. Miller. "THE P53 FAMILY MEMBER, P63, REGULATES NEURAL PRECURSOR CELL SURVIVAL DURING CORTICAL DEVELOPMENT." Clinical & Investigative Medicine 31, no. 4 (August 1, 2008): 8. http://dx.doi.org/10.25011/cim.v31i4.4799.

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Background: p63, a member of the p53 family of proteins, is involved in the regulation of naturally-occurring apoptosis in sympathetic neurons of the peripheral nervous system. Since data from our laboratory indicated that p63 is also expressed in stem cells and neurons within the developing brain, we hypothesized that p63 is involved in regulating the genesis and survival of developing neurons. Methods: As cortical neurogenesis is initiated at embryonic day 12, we knocked-down p63 levels in isolated murine cortical precursors byusing shRNA against p63 or by transfecting floxed-p63 precursors with Cre recombinase. We performed similar studies in vivo using in uteroelectroporation to express either p63 shRNA or Cre recombinase to acutely knockdown or genetically ablate p63. We then performed immunofluorescence for known markers of apoptosis, cell-division, and differentiation to assess the level of cell death, proliferation and neurogenesis. Results: Knock-down of p63 in vitro resulted in a 2-foldincrease in the death of precursors and neurons, associated with blunted neurogenesis but unaltered precursor proliferation. Coincident knock-down of p63 family members, p53, but not p73, rescued the elevated death suggesting that p63 and p53 antagonize each other to promote survival. Similar results were observed in vivo, where knockdown of p63 caused cell death and a decrease in the proportionof neurons in the cortical plate. Conclusions: These experiments indicate that p63 is required forthe survival of neural precursors and newly-born neurons, and for normal cortical development. Ongoing work will explore the environmental cues that regulate p63 during neurogenesis.

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Stricker, Priscila Elias Ferreira, Daiany de Souza Dobuchak, Ana Carolina Irioda, Bassam Felipe Mogharbel, Celia Regina Cavichiolo Franco, José Roberto de Souza Almeida Leite, Alyne Rodrigues de Araújo, et al. "Human Mesenchymal Stem Cells Seeded on the Natural Membrane to Neurospheres for Cholinergic-like Neurons." Membranes 11, no. 8 (August 7, 2021): 598. http://dx.doi.org/10.3390/membranes11080598.

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This study aimed to differentiate human mesenchymal stem cells (hMSCs) from the human umbilical cord in cholinergic-like neurons using a natural membrane. The isolation of hMSCs from Wharton’s jelly (WJ) was carried out using “explant” and mononuclear cells by the density gradient from umbilical blood and characterized by flow cytometry. hMSCs were seeded in a natural functional biopolymer membrane to produce neurospheres. RT-PCR was performed on hMSCs and neurospheres derived from the umbilical cord. Neural precursor cells were subjected to a standard cholinergic-like neuron differentiation protocol. Dissociated neurospheres, neural precursor cells, and cholinergic-like neurons were characterized by immunocytochemistry. hMSCs were CD73+, CD90+, CD105+, CD34- and CD45- and demonstrated the trilineage differentiation. Neurospheres and their isolated cells were nestin-positive and expressed NESTIN, MAP2, ßIII-TUBULIN, GFAP genes. Neural precursor cells that were differentiated in cholinergic-like neurons expressed ßIII-TUBULIN protein and choline acetyltransferase enzyme. hMSCs seeded on the natural membrane can differentiate into neurospheres, obtaining neural precursor cells without growth factors or gene transfection before cholinergic phenotype differentiation.

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Hudish, Laura I., and Bruce Appel. "microRNA regulation of neural precursor self-renewal and differentiation." Neurogenesis 1, no. 1 (January 2014): e976018. http://dx.doi.org/10.4161/23262133.2014.976018.

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Poulatsidou, Kyriaki-Nefeli, Roza Lagoudaki, Olga Touloumi, Evangelia Kesidou, Marina Boziki, Stylianos Ravanidis, Katerina Chlichlia, Maria Grigoriou, and Nikolaos Grigoriadis. "Immunophenotype of mouse cerebral hemispheres-derived neural precursor cells." Neuroscience Letters 611 (January 2016): 33–39. http://dx.doi.org/10.1016/j.neulet.2015.11.011.

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Adefuin, Aliya Mari D., Ayaka Kimura, Hirofumi Noguchi, Kinichi Nakashima, and Masakazu Namihira. "Epigenetic mechanisms regulating differentiation of neural stem/precursor cells." Epigenomics 6, no. 6 (December 2014): 637–49. http://dx.doi.org/10.2217/epi.14.53.

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Fike, John R., Susanna Rosi, and Charles L. Limoli. "Neural Precursor Cells and Central Nervous System Radiation Sensitivity." Seminars in Radiation Oncology 19, no. 2 (April 2009): 122–32. http://dx.doi.org/10.1016/j.semradonc.2008.12.003.

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Emery, B., T. D. Merson, C. Snell, K. M. Young, M. Ernst, and T. J. Kilpatrick. "SOCS3 negatively regulates LIF signaling in neural precursor cells." Molecular and Cellular Neuroscience 31, no. 4 (April 2006): 739–47. http://dx.doi.org/10.1016/j.mcn.2006.01.005.

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Furlan, Alessandro, and Igor Adameyko. "Schwann cell precursor: a neural crest cell in disguise?" Developmental Biology 444 (December 2018): S25—S35. http://dx.doi.org/10.1016/j.ydbio.2018.02.008.

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Vanderluit, Jacqueline L., Kerry L. Ferguson, Vassiliki Nikoletopoulou, Maura Parker, Vladimir Ruzhynsky, Tania Alexson, Stephen M. McNamara, David S. Park, Michael Rudnicki, and Ruth S. Slack. "p107 regulates neural precursor cells in the mammalian brain." Journal of Cell Biology 166, no. 6 (September 7, 2004): 853–63. http://dx.doi.org/10.1083/jcb.200403156.

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Here we show a novel function for Retinoblastoma family member, p107 in controlling stem cell expansion in the mammalian brain. Adult p107-null mice had elevated numbers of proliferating progenitor cells in their lateral ventricles. In vitro neurosphere assays revealed striking increases in the number of neurosphere forming cells from p107−/− brains that exhibited enhanced capacity for self-renewal. An expanded stem cell population in p107-deficient mice was shown in vivo by (a) increased numbers of slowly cycling cells in the lateral ventricles; and (b) accelerated rates of neural precursor repopulation after progenitor ablation. Notch1 was up-regulated in p107−/− neurospheres in vitro and brains in vivo. Chromatin immunoprecipitation and p107 overexpression suggest that p107 may modulate the Notch1 pathway. These results demonstrate a novel function for p107 that is distinct from Rb, which is to negatively regulate the number of neural stem cells in the developing and adult brain.

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Limoli, C. L., R. Rola, E. Giedzinski, S. Mantha, T. T. Huang, and J. R. Fike. "Cell-density-dependent regulation of neural precursor cell function." Proceedings of the National Academy of Sciences 101, no. 45 (November 2, 2004): 16052–57. http://dx.doi.org/10.1073/pnas.0407065101.

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Tyler, William A., Maria Medalla, Teresa Guillamon-Vivancos, Jennifer I. Luebke, and Tarik F. Haydar. "Neural Precursor Lineages Specify Distinct Neocortical Pyramidal Neuron Types." Journal of Neuroscience 35, no. 15 (April 15, 2015): 6142–52. http://dx.doi.org/10.1523/jneurosci.0335-15.2015.

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