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Journal articles on the topic 'Neurodifferentiation'

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Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Moreira, Natália Chermont dos Santos, Jéssica Ellen Barbosa de Freitas Lima, Talita Perez Cantuaria Chierrito, Ivone Carvalho, and Elza Tiemi Sakamoto-Hojo. "Novel Hybrid Acetylcholinesterase Inhibitors Induce Differentiation and Neuritogenesis in Neuronal Cells in vitro Through Activation of the AKT Pathway." Journal of Alzheimer's Disease 78, no. 1 (October 27, 2020): 353–70. http://dx.doi.org/10.3233/jad-200425.

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Background: Alzheimer’s disease (AD) is characterized by a progressive loss of episodic memory associated with amyloid-β peptide aggregation and the abnormal phosphorylation of the tau protein, leading to the loss of cholinergic function. Acetylcholinesterase (AChE) inhibitors are the main class of drugs used in AD therapy. Objective: The aim of the current study was to evaluate the potential of two tacrine-donepezil hybrid molecules (TA8Amino and TAHB3), which are AChE inhibitors, to induce neurodifferentiation and neuritogenesis in SH-SY5Y cells. Methods: The experiments were carried out to characterize neurodifferentiation, cellular changes related to responses to oxidative stress and pathways of cell survival in response to drug treatments. Results: The results indicated that the compounds did not present cytotoxic effects in SH-SY5Y or HepG2 cells. TA8Amino and TAHB3 induced neurodifferentiation and neuritogenesis in SH-SY5Y cells. These cells showed increased levels of intracellular and mitochondrial reactive oxygen species; the induction of oxidative stress was also demonstrated by an increase in SOD1 expression in TA8Amino and TAHB3-treated cells. Cells treated with the compounds showed an increase in PTEN(Ser380/Thr382/383) and AKT(Ser473) expression, suggesting the involvement of the AKT pathway. Conclusion: Our results demonstrated that TA8Amino and TAHB3 present advantages as potential drugs for AD therapy and that they are capable of inducing neurodifferentiation and neuritogenesis.

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2

Maffezzini, Camilla, Javier Calvo-Garrido, Anna Wredenberg, and Christoph Freyer. "Metabolic regulation of neurodifferentiation in the adult brain." Cellular and Molecular Life Sciences 77, no. 13 (January 7, 2020): 2483–96. http://dx.doi.org/10.1007/s00018-019-03430-9.

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AbstractUnderstanding the mechanisms behind neurodifferentiation in adults will be an important milestone in our quest to identify treatment strategies for cognitive disorders observed during our natural ageing or disease. It is now clear that the maturation of neural stem cells to neurones, fully integrated into neuronal circuits requires a complete remodelling of cellular metabolism, including switching the cellular energy source. Mitochondria are central for this transition and are increasingly seen as the regulatory hub in defining neural stem cell fate and neurodevelopment. This review explores our current knowledge of metabolism during adult neurodifferentiation.

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3

Huang, Min, Xiaoxiao Xiao, Guanxu Ji, and Qiang Wu. "Histone modifications in neurodifferentiation of embryonic stem cells." Heliyon 8, no. 1 (January 2022): e08664. http://dx.doi.org/10.1016/j.heliyon.2021.e08664.

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4

Belinsky, Glenn S., Carissa L. Sirois, Matthew T. Rich, Shaina M. Short, Anna R. Moore, Sarah E. Gilbert, and Srdjan D. Antic. "Dopamine Receptors in Human Embryonic Stem Cell Neurodifferentiation." Stem Cells and Development 22, no. 10 (May 15, 2013): 1522–40. http://dx.doi.org/10.1089/scd.2012.0150.

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5

Qutub, Amina Ann, Erin Pollet, Byron Long, Arun Mahadevan, and George Britton. "DIGITIZING BRAIN HEALTH: FROM NEURODIFFERENTIATION TO DAILY ACTIVITIES." Alzheimer's & Dementia 15, no. 7 (July 2019): P161. http://dx.doi.org/10.1016/j.jalz.2019.06.4330.

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6

Slotkin, Theodore A., and Frederic J. Seidler. "Benzo[a]pyrene impairs neurodifferentiation in PC12 cells." Brain Research Bulletin 80, no. 1-2 (August 2009): 17–21. http://dx.doi.org/10.1016/j.brainresbull.2009.06.003.

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7

Blando, Santino, Ivana Raffaele, Luigi Chiricosta, Andrea Valeri, Agnese Gugliandolo, Serena Silvestro, Federica Pollastro, and Emanuela Mazzon. "Cannabidiol Promotes Neuronal Differentiation Using Akt and Erk Pathways Triggered by Cb1 Signaling." Molecules 27, no. 17 (September 1, 2022): 5644. http://dx.doi.org/10.3390/molecules27175644.

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Recently, the scientific community has started to focus on the neurogenic potential of cannabinoids. The phytocompound cannabidiol (CBD) shows different mechanism of signaling on cannabinoid receptor 1 (CB1), depending on its concentration. In this study, we investigated if CBD may induce in vitro neuronal differentiation after treatment at 5 µM and 10 µM. For this purpose, we decided to use the spinal cord × neuroblastoma hybrid cell line (NSC-34) because of its proliferative and undifferentiated state. The messenger RNAs (mRNAs) expression profiles were tested using high-throughput sequencing technology and Western blot assay was used to determine the number of main proteins in different pathways. Interestingly, the treatment shows different genes associated with neurodifferentiation statistically significant, such as Rbfox3, Tubb3, Pax6 and Eno2. The CB1 signaling pathway is responsible for neuronal differentiation at 10 µM, as suggested by the presence of p-ERK and p-AKT, but not at 5 µM. A new correlation between CBD, neurodifferentiation and retinoic acid receptor-related orphan receptors (RORs) has been observed.

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Parfejevs, V., M. Gavare, L. Cappiello, M. Grube, R. Muceniece, and U. Riekstina. "Evaluation of Biochemical Changes in Skin-Derived Mesenchymal Stem Cells duringIn VitroNeurodifferentiation by FT-IR Analysis." Spectroscopy: An International Journal 27 (2012): 315–20. http://dx.doi.org/10.1155/2012/286542.

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Recently FT-IR analysis has been employed to study changes in molecular signatures during embryonic stem cell differentiation. We were interested to find out whether FT-IR spectroscopy could be applied to analyze changes in human skin mesenchymal stem cell (S-MSC) biochemical profile duringin vitroneurodifferentiation. S-MSCs were propagated in serum-free medium with EGF and FGF-2 during six weeks. Neural progenitor cell line ReNcell CX (Millipore) was used as a reference cell line. Samples were collected each week and analyzed for neural marker nestin, tubulinβIII, GFAP, and CD271 expression. FT-IR analysis was carried out using microplate reader HTS-XT (Bruker, Germany). Despite the immunophenotype similarity, FT-IR spectroscopy revealed distinct profiles for S-MSC culture and ReNcell CX cells. FT-IR spectra analyses showed changes of protein and lipid concentration during neurodifferentiation and different carbohydrate composition in ReNcell CX and S-MSCs. It was possible to discriminate between S-MSC cultures at different time points during neurodifferentiation. The results of this study demonstrate that FT-IR spectroscopy is more sensitive than conventional immunophenotyping analysis and it has a great potential for the monitoring of the stem cell differentiation status.

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9

Hsu, Wei-Hsiang, Nai-Kuei Huang, Young-Ji Shiao, Chung-Kuang Lu, Yen-Ming Chao, Yi-Jeng Huang, Chih-Hsin Yeh, and Yun-Lian Lin. "Gastrodiae rhizoma attenuates brain aging via promoting neuritogenesis and neurodifferentiation." Phytomedicine 87 (July 2021): 153576. http://dx.doi.org/10.1016/j.phymed.2021.153576.

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10

Lai, Bin, Xiao Ou Mao, Lin Xie, Kunlin Jin, and David A. Greenberg. "Electrophysiological neurodifferentiation of subventricular zone-derived precursor cells following stroke." Neuroscience Letters 442, no. 3 (September 2008): 305–8. http://dx.doi.org/10.1016/j.neulet.2008.07.032.

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11

Calvo-Garrido, Javier, Camilla Maffezzini, Florian A. Schober, Paula Clemente, Elias Uhlin, Malin Kele, Henrik Stranneheim, et al. "SQSTM1/p62-Directed Metabolic Reprogramming Is Essential for Normal Neurodifferentiation." Stem Cell Reports 12, no. 4 (April 2019): 696–711. http://dx.doi.org/10.1016/j.stemcr.2019.01.023.

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12

Sobel, Raymond A., Mary Jane Eaton, Prajakta Dilip Jaju, Eugene Lowry, and Julian R. Hinojoza. "Anti-Myelin Proteolipid Protein Peptide Monoclonal Antibodies Recognize Cell Surface Proteins on Developing Neurons and Inhibit Their Differentiation." Journal of Neuropathology & Experimental Neurology 78, no. 9 (August 10, 2019): 819–43. http://dx.doi.org/10.1093/jnen/nlz058.

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Abstract Using a panel of monoclonal antibodies (mAbs) to myelin proteolipid protein (PLP) peptides, we found that in addition to CNS myelin, mAbs to external face but not cytoplasmic face epitopes immunostained neurons in immature human CNS tissues and in adult hippocampal dentate gyrus and olfactory bulbs, that is neural stem cell niches (NSCN). To explore the pathobiological significance of these observations, we assessed the mAb effects on neurodifferentiation in vitro. The mAbs to PLP 50–69 (IgG1κ and IgG2aκ), and 178–191 and 200–219 (both IgG1κ) immunostained live cell surfaces and inhibited neurite outgrowth of E18 rat hippocampal precursor cells and of PC12 cells, which do not express PLP. Proteins immunoprecipitated from PC12 cell extracts and captured by mAb-coated magnetic beads were identified by GeLC-MS/MS. Each neurite outgrowth-inhibiting mAb captured a distinct set of neurodifferentiation molecules including sequence-similar M6 proteins and other unrelated membrane and extracellular matrix proteins, for example integrins, Eph receptors, NCAM-1, and protocadherins. These molecules are expressed in adult human NSCN and are implicated in the pathogenesis of many chronic CNS disease processes. Thus, diverse anti-PLP epitope autoantibodies may inhibit neuronal precursor cell differentiation via multispecific recognition of cell surface molecules thereby potentially impeding endogenous neuroregeneration in NSCN and in vivo differentiation of exogenous neural stem cells.

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13

Galigniana, MarioD, and Cristina Daneri-Becerra. "The Hsp90-binding immunophilin FKBP52 enhances neurodifferentiation and neuroregeneration in murine models." Neural Regeneration Research 17, no. 3 (2022): 555. http://dx.doi.org/10.4103/1673-5374.320976.

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14

Xu, Ruodan, Maxime Feyeux, Stéphanie Julien, Csilla Nemes, Morten Albrechtsen, Andras Dinnyés, and Karl-Heinz Krause. "Screening of Bioactive Peptides Using an Embryonic Stem Cell-Based Neurodifferentiation Assay." AAPS Journal 16, no. 3 (February 21, 2014): 400–412. http://dx.doi.org/10.1208/s12248-014-9578-7.

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15

Allende, Maria L., Emily K. Cook, Bridget C. Larman, Adrienne Nugent, Jacqueline M. Brady, Diane Golebiowski, Miguel Sena-Esteves, Cynthia J. Tifft, and Richard L. Proia. "Cerebral organoids derived from Sandhoff disease-induced pluripotent stem cells exhibit impaired neurodifferentiation." Journal of Lipid Research 59, no. 3 (January 22, 2018): 550–63. http://dx.doi.org/10.1194/jlr.m081323.

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16

Slotkin, Theodore A., and Frederic J. Seidler. "Does mechanism matter? Unrelated neurotoxicants converge on cell cycle and apoptosis during neurodifferentiation." Neurotoxicology and Teratology 34, no. 4 (July 2012): 395–402. http://dx.doi.org/10.1016/j.ntt.2012.04.008.

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17

Fernandez Garcia-Agudo, Laura, Agnes A. Steixner-Kumar, Yasmina Curto, Nadine Barnkothe, Imam Hassouna, Sebastian Jähne, Umer Javed Butt, et al. "Brain erythropoietin fine-tunes a counterbalance between neurodifferentiation and microglia in the adult hippocampus." Cell Reports 36, no. 8 (August 2021): 109548. http://dx.doi.org/10.1016/j.celrep.2021.109548.

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18

Tsai, Eing-Mei, Yu-Chih Wang, Tony Tung-Yin Lee, Cheng-Fang Tsai, Hung-Sheng Chen, Feng-Jie Lai, Kazunari K. Yokoyama, Tsung-Hsun Hsieh, Ruey-Meei Wu, and Jau-nan Lee. "Dynamic Trk and G Protein Signalings Regulate Dopaminergic Neurodifferentiation in Human Trophoblast Stem Cells." PLOS ONE 10, no. 11 (November 25, 2015): e0143852. http://dx.doi.org/10.1371/journal.pone.0143852.

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19

Slotkin, Theodore A., and Frederic J. Seidler. "Developmental neurotoxicants target neurodifferentiation into the serotonin phenotype: Chlorpyrifos, diazinon, dieldrin and divalent nickel." Toxicology and Applied Pharmacology 233, no. 2 (December 2008): 211–19. http://dx.doi.org/10.1016/j.taap.2008.08.020.

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20

Simonovic, Jelena, Bosko Toljic, Milos Lazarevic, Maja Milosevic Markovic, Mina Peric, Jasna Vujin, Radmila Panajotovic, and Jelena Milasin. "The Effect of Liquid-Phase Exfoliated Graphene Film on Neurodifferentiation of Stem Cells from Apical Papilla." Nanomaterials 12, no. 18 (September 8, 2022): 3116. http://dx.doi.org/10.3390/nano12183116.

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Background: Dental stem cells, which originate from the neural crest, due to their easy accessibility might be good candidates in neuro-regenerative procedures, along with graphene-based nanomaterials shown to promote neurogenesis in vitro. We aimed to explore the potential of liquid-phase exfoliated graphene (LPEG) film to stimulate the neuro-differentiation of stem cells from apical papilla (SCAP). Methods: The experimental procedure was structured as follows: (1) fabrication of graphene film; (2) isolation, cultivation and SCAP stemness characterization by flowcytometry, multilineage differentiation (osteo, chondro and adipo) and quantitative PCR (qPCR); (3) SCAP neuro-induction by cultivation on polyethylene terephthalate (PET) coated with graphene film; (4) evaluation of neural differentiation by means of several microscopy techniques (light, confocal, atomic force and scanning electron microscopy), followed by neural marker gene expression analysis using qPCR. Results: SCAP demonstrated exceptional stemness, as judged by mesenchymal markers’ expression (CD73, CD90 and CD105), and by multilineage differentiation capacity (osteo, chondro and adipo-differentiation). Neuro-induction of SCAP grown on PET coated with graphene film resulted in neuron-like cellular phenotype observed under different microscopes. This was corroborated by the high gene expression of all examined key neuronal markers (Ngn2, NF-M, Nestin, MAP2, MASH1). Conclusions: The ability of SCAPs to differentiate toward neural lineages was markedly enhanced by graphene film.

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21

Heng, Julian, ZhengDong Qu, Francois Guillemot, and Seong-Seng Tan. "Negative feedback regulation of a proneural bHLH program for neurodifferentiation by a zinc finger transcription factor." Neuroscience Research 65 (January 2009): S56. http://dx.doi.org/10.1016/j.neures.2009.09.138.

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22

Slotkin, Theodore A., Samantha Skavicus, Jennifer Card, Edward D. Levin, and Frederic J. Seidler. "Amelioration strategies fail to prevent tobacco smoke effects on neurodifferentiation: Nicotinic receptor blockade, antioxidants, methyl donors." Toxicology 333 (July 2015): 63–75. http://dx.doi.org/10.1016/j.tox.2015.04.005.

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23

Dar, Mohd Ishaq, Priya Mahajan, Suraya Jan, Shreyans K. Jain, Harshita Tiwari, Jagjeet Sandey, Sandip Bharate, Amit Nargotra, and Sajad Hussain Syed. "Rottlerin is a pan phosphodiesterase inhibitor and can induce neurodifferentiation in IMR-32 human neuroblastoma cells." European Journal of Pharmacology 857 (August 2019): 172448. http://dx.doi.org/10.1016/j.ejphar.2019.172448.

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24

Mak, Sally K., Y. Anne Huang, Shifteh Iranmanesh, Malini Vangipuram, Ramya Sundararajan, Loan Nguyen, J. William Langston, and Birgitt Schüle. "Small Molecules Greatly Improve Conversion of Human-Induced Pluripotent Stem Cells to the Neuronal Lineage." Stem Cells International 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/140427.

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Efficientin vitrodifferentiation into specific cell types is more important than ever after the breakthrough in nuclear reprogramming of somatic cells and its potential for disease modeling and drug screening. Key success factors for neuronal differentiation are the yield of desired neuronal marker expression, reproducibility, length, and cost. Three main neuronal differentiation approaches are stromal-induced neuronal differentiation, embryoid body (EB) differentiation, and direct neuronal differentiation. Here, we describe our neurodifferentiation protocol using small molecules that very efficiently promote neural induction in a 5-stage EB protocol from six induced pluripotent stem cells (iPSC) lines from patients with Parkinson’s disease and controls. This protocol generates neural precursors using Dorsomorphin and SB431542 and further maturation into dopaminergic neurons by replacing sonic hedgehog with purmorphamine or smoothened agonist. The advantage of this approach is that all patient-specific iPSC lines tested in this study were successfully and consistently coaxed into the neural lineage.

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Natale, Francesca, Matteo Spinelli, Saviana Antonella Barbati, Lucia Leone, Salvatore Fusco, and Claudio Grassi. "High Fat Diet Multigenerationally Affects Hippocampal Neural Stem Cell Proliferation via Epigenetic Mechanisms." Cells 11, no. 17 (August 27, 2022): 2661. http://dx.doi.org/10.3390/cells11172661.

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Early-life metabolic stress has been demonstrated to affect brain development, persistently influence brain plasticity and to exert multigenerational effects on cognitive functions. However, the impact of an ancestor’s diet on the adult neurogenesis of their descendants has not yet been investigated. Here, we studied the effects of maternal high fat diet (HFD) on hippocampal adult neurogenesis and the proliferation of neural stem and progenitor cells (NSPCs) derived from the hippocampus of both the second and the third generations of progeny (F2HFD and F3HFD). Maternal HFD caused a multigenerational depletion of neurogenic niche in F2HFD and F3HFD mice. Moreover, NSPCs derived from HFD descendants showed altered expression of genes regulating stem cell proliferation and neurodifferentiation (i.e., Hes1, NeuroD1, Bdnf). Finally, ancestor HFD-related hyper-activation of both STAT3 and STAT5 induced enhancement of their binding on the regulatory sequences of Gfap gene and an epigenetic switch from permissive to repressive chromatin on the promoter of the NeuroD1 gene. Collectively, our data indicate that maternal HFD multigenerationally affects hippocampal adult neurogenesis via an epigenetic derangement of pro-neurogenic gene expression in NSPCs.

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Malheiro, R. F., H. Carmo, F. Carvalho, and J. P. Silva. "P16-10 The synthetic cannabinoid ADB-FUBINACA modulates mitochondrial activity and dynamics during neurodifferentiation of NG108-15 cells." Toxicology Letters 368 (September 2022): S221—S222. http://dx.doi.org/10.1016/j.toxlet.2022.07.600.

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27

Slotkin, Theodore A., Jennifer Card, Ashley Stadler, Edward D. Levin, and Frederic J. Seidler. "Effects of tobacco smoke on PC12 cell neurodifferentiation are distinct from those of nicotine or benzo[a]pyrene." Neurotoxicology and Teratology 43 (May 2014): 19–24. http://dx.doi.org/10.1016/j.ntt.2014.03.002.

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28

Pamies, D., A. Bal-Price, M. Fabbri, L. Gribaldo, B. Scelfo, G. Harris, A. Collotta, E. Vilanova, and M. A. Sogorb. "Silencing of PNPLA6, the neuropathy target esterase (NTE) codifying gene, alters neurodifferentiation of human embryonal carcinoma stem cells (NT2)." Neuroscience 281 (December 2014): 54–67. http://dx.doi.org/10.1016/j.neuroscience.2014.08.031.

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29

Logotheti, Stella, Stephan Marquardt, Christin Richter, Renée Sophie Hain, Nico Murr, Işıl Takan, Athanasia Pavlopoulou, and Brigitte M. Pützer. "Neural Networks Recapitulation by Cancer Cells Promotes Disease Progression: A Novel Role of p73 Isoforms in Cancer-Neuronal Crosstalk." Cancers 12, no. 12 (December 16, 2020): 3789. http://dx.doi.org/10.3390/cancers12123789.

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Mechanisms governing tumor progression differ from those of initiation. One enigmatic prometastatic process is the recapitulation of pathways of neural plasticity in aggressive stages. Cancer and neuronal cells develop reciprocal interactions via mutual production and secretion of neuronal growth factors, neurothrophins and/or axon guidance molecules in the tumor microenvironment. Understanding cancer types where this process is active, as well as the drivers, markers and underlying mechanisms, has great significance for blocking tumor progression and improving patient survival. By applying computational and systemic approaches, in combination with experimental validations, we provide compelling evidence that genes involved in neuronal development, differentiation and function are reactivated in tumors and predict poor patient outcomes across various cancers. Across cancers, they co-opt genes essential for the development of distinct anatomical parts of the nervous system, with a frequent preference for cerebral cortex and neural crest-derived enteric nerves. Additionally, we show that p73, a transcription factor with a dual role in neuronal development and cancer, simultaneously induces neurodifferentiation and stemness markers during melanoma progression. Our data yield the basis for elucidating driving forces of the nerve–tumor cell crosstalk and highlight p73 as a promising regulator of cancer neurobiology.

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30

Tirpáková, Mária, Jaromír Vašíček, Andrea Svoradová, Andrej Baláži, Marián Tomka, Miroslav Bauer, Alexander Makarevich, and Peter Chrenek. "Phenotypical Characterization and Neurogenic Differentiation of Rabbit Adipose Tissue-Derived Mesenchymal Stem Cells." Genes 12, no. 3 (March 17, 2021): 431. http://dx.doi.org/10.3390/genes12030431.

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Although the rabbit is a frequently used biological model, the phenotype of rabbit adipose-derived mesenchymal stem cells (rAT-MSCs) is not well characterized. One of the reasons is the absence of specific anti-rabbit antibodies. The study aimed to characterize rAT-MSCs using flow cytometry and PCR methods, especially digital droplet PCR, which confirmed the expression of selected markers at the mRNA level. A combination of these methods validated the expression of MSCs markers (CD29, CD44, CD73, CD90 and CD105). In addition, cells were also positive for CD49f, vimentin, desmin, α-SMA, ALDH and also for the pluripotent markers: NANOG, OCT4 and SOX2. Moreover, the present study proved the ability of rAT-MSCs to differentiate into a neurogenic lineage based on the confirmed expression of neuronal markers ENO2 and MAP2. Obtained results suggest that rAT-MSCs have, despite the slight differences in marker expression, the similar phenotype as human AT-MSCs and possess the neurodifferentiation ability. Accordingly, rAT-MSCs should be subjected to further studies with potential application in veterinary medicine but also, in case of their cryopreservation, as a source of genetic information of endangered species stored in the gene bank.

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31

Ge, Gaoxiang, Delana R. Hopkins, Wen-Bin Ho, and Daniel S. Greenspan. "GDF11 Forms a Bone Morphogenetic Protein 1-Activated Latent Complex That Can Modulate Nerve Growth Factor-Induced Differentiation of PC12 Cells." Molecular and Cellular Biology 25, no. 14 (July 2005): 5846–58. http://dx.doi.org/10.1128/mcb.25.14.5846-5858.2005.

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ABSTRACT All transforming growth factor β (TGF-β) superfamily members are synthesized as precursors with prodomain sequences that are proteolytically removed by subtilisin-like proprotein convertases (SPCs). For most superfamily members, this is believed sufficient for activation. Exceptions are TGF-βs 1 to 3 and growth differentiation factor 8 (GDF8), also known as myostatin, which form noncovalent, latent complexes with their SPC-cleaved prodomains. Sequence similarities between TGF-βs 1 to 3, myostatin, and superfamily member GDF11, also known as bone morphogenetic protein 11 (BMP11), prompted us to examine whether GDF11 might be capable of forming a latent complex with its cleaved prodomain. Here we demonstrate that GDF11 forms a noncovalent latent complex with its SPC-cleaved prodomain and that this latent complex is activated via cleavage at a single specific site by members of the developmentally important BMP1/Tolloid family of metalloproteinases. Evidence is provided for a molecular model whereby formation and activation of this complex may play a general role in modulating neural differentiation. In particular, mutant GDF11 prodomains impervious to cleavage by BMP1/Tolloid proteinases are shown to be potent stimulators of neurodifferentiation, with potential for therapeutic applications.

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Ke, Tao, Alexey A. Tinkov, Anatoly V. Skalny, Abel Santamaria, Joao B. T. Rocha, Aaron B. Bowman, Wen Chen, and Michael Aschner. "Epigenetics and Methylmercury-Induced Neurotoxicity, Evidence from Experimental Studies." Toxics 11, no. 1 (January 12, 2023): 72. http://dx.doi.org/10.3390/toxics11010072.

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MeHg is an environmental neurotoxin that can adversely affect the development of the nervous system. The molecular integrity of chromatin in the nucleus is an important target of MeHg. Low levels of MeHg trigger epigenetic mechanisms that may be involved in long-lasting and transgenerational neurotoxicity after exposure. Emerging evidence has shown that these mechanisms include histone modification, siRNA, and DNA methylation. The MeHg-induced inhibition of neurodifferentiation and neurogenesis are mechanistically associated with epigenetic alterations in critical genes, such as neurotrophin brain-derived neurotrophic factor (BDNF). Further, MeHg exposure has been shown to alter the activity and/or expression of the upstream regulators of chromatin structure, including histone deacetylases (HDACs) and DNA methyltransferase (DNMTs), which may trigger permanent alterations in histone modifications and DNA methylation. MeHg-exposure also alters several species of miRNA that are associated with neurodevelopment. Genetic studies in the C. elegans model of MeHg-induced toxicity proposes a potential interplay between exogenous RNAi and antioxidant defense. In this review, we discuss the molecular basis for MeHg exposure-induced alterations in chromatin structure and the roles of histone modifications, siRNA, and DNA methylation in MeHg-induced neurotoxic effects.

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33

Malheiro, R. F., H. Carmo, F. Félix Carvalho, and J. P. Silva. "In vitro evaluation of the effects of the synthetic cannabinoids ADB-FUBINACA and AMB-FUBINACA on mitochondrial function during neurodifferentiation." Toxicology Letters 350 (September 2021): S140. http://dx.doi.org/10.1016/s0378-4274(21)00572-5.

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34

Alexandre, João, Rui Malheiro, Diana Dias da Silva, Helena Carmo, Félix Carvalho, and João Pedro Silva. "The Synthetic Cannabinoids THJ-2201 and 5F-PB22 Enhance In Vitro CB1 Receptor-Mediated Neuronal Differentiation at Biologically Relevant Concentrations." International Journal of Molecular Sciences 21, no. 17 (August 30, 2020): 6277. http://dx.doi.org/10.3390/ijms21176277.

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Recreational use of synthetic cannabinoids (SCs) before and during pregnancy poses a major public health risk, due to the potential onset of neurodevelopmental disorders in the offspring. Herein, we report the assessment of the neurotoxic potential of two commonly abused SCs, THJ-2201 and 5F-PB22, particularly focusing on how they affect neuronal differentiation in vitro. Differentiation ratios, total neurite length, and neuronal marker expression were assessed in NG108-15 neuroblastoma x glioma cells exposed to the SCs at non-toxic, biologically relevant concentrations (≤1 μM), either in acute or repeated exposure settings. Both SCs enhanced differentiation ratios and total neurite length of NG108-15 cells near two-fold compared to vehicle-treated cells, in a CB1R activation-dependent way, as the CB1R blockade with a specific antagonist (SR141718) abrogated SC-induced effects. Interestingly, repeated 5F-PB22 exposure was required to reach effects similar to a single THJ-2201 dose. Cell viability and proliferation, mitochondrial membrane potential, and intracellular ATP levels were also determined. The tested SCs increased mitochondrial tetramethyl rhodamine ethyl ester (TMRE) accumulation after 24 h at biologically relevant concentrations but did not affect any of the other toxicological parameters. Overall, we report firsthand the CB1R-mediated enhancement of neurodifferentiation by 5F-PB22 and THJ-2201 at biologically relevant concentrations.

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35

Zloh, Miloslav, Patrik Kutilek, and Andrea Stofkova. "High-Contrast Stimulation Potentiates the Neurotrophic Properties of Müller Cells and Suppresses Their Pro-Inflammatory Phenotype." International Journal of Molecular Sciences 23, no. 15 (August 3, 2022): 8615. http://dx.doi.org/10.3390/ijms23158615.

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High-contrast visual stimulation promotes retinal regeneration and visual function, but the underlying mechanism is not fully understood. Here, we hypothesized that Müller cells (MCs), which express neurotrophins such as brain-derived neurotrophic factor (BDNF), could be key players in this retinal plasticity process. This hypothesis was tested by conducting in vivo and in vitro high-contrast stimulation of adult mice and MCs. Following stimulation, we examined the expression of BDNF and its inducible factor, VGF, in the retina and MCs. We also investigated the alterations in the expression of VGF, nuclear factor kappa B (NF-κB) and pro-inflammatory mediators in MCs, as well as their capacity to proliferate and develop a neurogenic or reactive gliosis phenotype after high-contrast stimulation and treatment with BDNF. Our results showed that high-contrast stimulation upregulated BDNF levels in MCs in vivo and in vitro. The additional BDNF treatment significantly augmented VGF production in MCs and their neuroprotective features, as evidenced by increased MC proliferation, neurodifferentiation, and decreased expression of the pro-inflammatory factors and the reactive gliosis marker GFAP. These results demonstrate that high-contrast stimulation activates the neurotrophic and neuroprotective properties of MCs, suggesting their possible direct involvement in retinal neuronal survival and improved functional outcomes in response to visual stimulation.

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Liu, Xiaolu, Zhitao Feng, Lipeng Du, Yaguang Huang, Jinwen Ge, Yihui Deng, and Zhigang Mei. "The Potential Role of MicroRNA-124 in Cerebral Ischemia Injury." International Journal of Molecular Sciences 21, no. 1 (December 23, 2019): 120. http://dx.doi.org/10.3390/ijms21010120.

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Cerebral ischemia injury, the leading cause of morbidity and mortality worldwide, initiates sequential molecular and cellular pathologies that underlie ischemic encephalopathy (IE), such as ischemic stroke, Alzheimer disease (AD), Parkinson’s disease (PD), epilepsy, etc. Targeted therapeutic treatments are urgently needed to tackle the pathological processes implicated in these neurological diseases. Recently, accumulating studies demonstrate that microRNA-124 (miR-124), the most abundant miRNA in brain tissue, is aberrant in peripheral blood and brain vascular endothelial cells following cerebral ischemia. Importantly, miR-124 regulates a variety of pathophysiological processes that are involved in the pathogenesis of age-related IE. However, the role of miR-124 has not been systematically illustrated. Paradoxically, miR-124 exerts beneficial effects in the age-related IE via regulating autophagy, neuroinflammation, oxidative stress, neuronal excitability, neurodifferentiation, Aβ deposition, and hyperphosphorylation of tau protein, while it may play a dual role via regulating apoptosis and exerts detrimental effects on synaptic plasticity and axonal growth. In the present review, we thus focus on the paradoxical roles of miR-124 in age-related IE, as well as the underlying mechanisms. A great understanding of the effects of miR-124 on the hypoxic–ischemic brain will open new avenues for therapeutic approaches to protect against cerebral ischemia injury.

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Chan, S. Y., A. Martín-Santos, L. S. Loubière, A. M. González, B. Stieger, A. Logan, C. J. McCabe, J. A. Franklyn, and M. D. Kilby. "The expression of thyroid hormone transporters in the human fetal cerebral cortex during early development and in N-Tera-2 neurodifferentiation." Journal of Physiology 589, no. 11 (June 1, 2011): 2827–45. http://dx.doi.org/10.1113/jphysiol.2011.207290.

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Marinowic, D. R., M. F. Domingues, D. C. Machado, and J. C. DaCosta. "The expression of pluripotency genes and neuronal markers after neurodifferentiation in fibroblasts co-cultured with human umbilical cord blood mononuclear cells." In Vitro Cellular & Developmental Biology - Animal 51, no. 1 (August 19, 2014): 26–35. http://dx.doi.org/10.1007/s11626-014-9804-8.

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Dong, Mengqi, Yuanyuan Li, Min Zhu, Jinbo Li, and Zhanfen Qin. "Tetrabromobisphenol A Disturbs Brain Development in Both Thyroid Hormone-Dependent and -Independent Manners in Xenopus laevis." Molecules 27, no. 1 (December 31, 2021): 249. http://dx.doi.org/10.3390/molecules27010249.

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Although tetrabromobisphenol A (TBBPA) has been well proven to disturb TH signaling in both in vitro and in vivo assays, it is still unclear whether TBBPA can affect brain development due to TH signaling disruption. Here, we employed the T3-induced Xenopus metamorphosis assay (TIXMA) and the spontaneous metamorphosis assay to address this issue. In the TIXMA, 5–500 nmol/L TBBPA affected T3-induced TH-response gene expression and T3-induced brain development (brain morphological changes, cell proliferation, and neurodifferentiation) at premetamorphic stages in a complicated biphasic concentration-response manner. Notably, 500 nmol/L TBBPA treatment alone exerted a stimulatory effect on tadpole growth and brain development at these stages, in parallel with a lack of TH signaling activation, suggesting the involvement of other signaling pathways. As expected, at the metamorphic climax, we observed inhibitory effects of 50–500 nmol/L TBBPA on metamorphic development and brain development, which was in agreement with the antagonistic effects of higher concentrations on T3-induced brain development at premetamorphic stages. Taken together, all results demonstrate that TBBPA can disturb TH signaling and subsequently interfere with TH-dependent brain development in Xenopus; meanwhile, other signaling pathways besides TH signaling could be involved in this process. Our study improves the understanding of the effects of TBBPA on vertebrate brain development.

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Slotkin, Theodore A., Jennifer Card, and Frederic J. Seidler. "Adverse Benzo[ a ]pyrene Effects on Neurodifferentiation Are Altered by Other Neurotoxicant Coexposures: Interactions with Dexamethasone, Chlorpyrifos, or Nicotine in PC12 Cells." Environmental Health Perspectives 121, no. 7 (July 2013): 825–31. http://dx.doi.org/10.1289/ehp.1306528.

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Serra, Sofia C., João C. Costa, Rita C. Assunção-Silva, Fábio G. Teixeira, Nuno A. Silva, Sandro I. Anjo, Bruno Manadas, Jeffrey M. Gimble, Leo A. Behie, and António J. Salgado. "Influence of passage number on the impact of the secretome of adipose tissue stem cells on neural survival, neurodifferentiation and axonal growth." Biochimie 155 (December 2018): 119–28. http://dx.doi.org/10.1016/j.biochi.2018.09.012.

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Paley, Elena L. "Tryptamine-Induced Tryptophanyl-tRNAtrp Deficiency in Neurodifferentiation and Neurodegeneration Interplay: Progenitor Activation with Neurite Growth Terminated in Alzheimer's Disease Neuronal Vesicularization and Fragmentation." Journal of Alzheimer's Disease 26, no. 2 (September 9, 2011): 263–98. http://dx.doi.org/10.3233/jad-2011-110176.

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Mocanu-Dobranici, Alexandra-Elena, Marieta Costache, and Sorina Dinescu. "Insights into the Molecular Mechanisms Regulating Cell Behavior in Response to Magnetic Materials and Magnetic Stimulation in Stem Cell (Neurogenic) Differentiation." International Journal of Molecular Sciences 24, no. 3 (January 19, 2023): 2028. http://dx.doi.org/10.3390/ijms24032028.

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Magnetic materials and magnetic stimulation have gained increasing attention in tissue engineering (TE), particularly for bone and nervous tissue reconstruction. Magnetism is utilized to modulate the cell response to environmental factors and lineage specifications, which involve complex mechanisms of action. Magnetic fields and nanoparticles (MNPs) may trigger focal adhesion changes, which are further translated into the reorganization of the cytoskeleton architecture and have an impact on nuclear morphology and positioning through the activation of mechanotransduction pathways. Mechanical stress induced by magnetic stimuli translates into an elongation of cytoskeleton fibers, the activation of linker in the nucleoskeleton and cytoskeleton (LINC) complex, and nuclear envelope deformation, and finally leads to the mechanical regulation of chromatin conformational changes. As such, the internalization of MNPs with further magnetic stimulation promotes the evolution of stem cells and neurogenic differentiation, triggering significant changes in global gene expression that are mediated by histone deacetylases (e.g., HDAC 5/11), and the upregulation of noncoding RNAs (e.g., miR-106b~25). Additionally, exposure to a magnetic environment had a positive influence on neurodifferentiation through the modulation of calcium channels’ activity and cyclic AMP response element-binding protein (CREB) phosphorylation. This review presents an updated and integrated perspective on the molecular mechanisms that govern the cellular response to magnetic cues, with a special focus on neurogenic differentiation and the possible utility of nervous TE, as well as the limitations of using magnetism for these applications.

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Das, Debisukti, Utsav Mukherjee, Bibaswan Basu, and Devashish Sen. "Impact of thousand-and-one amino acid 2 kinase mediated neurodifferentiation in cerebral cortex and impairment of mirror neuron pathways on autism spectrum disorders." National Journal of Physiology, Pharmacy and Pharmacology 7, no. 4 (2017): 1. http://dx.doi.org/10.5455/njppp.2017.7.1235202012017.

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Tanner, Georgette, Martina A. Finetti, Steven Pollock, Nora Rippaus, Alexander-Francisco Bruns, Catherine Hogg, Alastair Droop, et al. "IDHwt Glioblastomas Show Opposing Resistance Mechanisms Across Patients in Response to Standard Treatment." Neuro-Oncology 24, Supplement_4 (October 1, 2022): iv1. http://dx.doi.org/10.1093/neuonc/noac200.000.

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Abstract AIMS Glioblastoma (GBM) is the most common primary malignant brain tumour in adults. Despite aggressive treatment, a resistant tumour recurs in practically all patients. We therefore aimed to better understand the mechanisms driving this treatment resistance through investigating changes in gene expression across pairs of primary and recurrent GBM tumours. METHOD We generated or acquired bulk tumour RNA sequencing data for primary and first recurrent tumours from 107 patients who received standard treatment. Differential expression analysis between primary and recurrent samples found that the most dysregulated genes were involved in neurodevelopment and neurodifferentiation. We therefore used a publicly available ChIP-seq database to identify DNA binding factors for which binding sites are enriched in the promotors of genes with the largest expression changes from primary to recurrent. RESULTS Jumonji and AT-Rich Interacting Domain 2 (JARID2) was the most strongly enriched for binding to promotors of dysregulated genes. 65 patients showed an up-regulation and 42 showed a down-regulation of genes bound by this protein. The same set of JARID2 bound genes were found to be dysregulated in each direction, and correlated with the largest source of variation between samples in their response to treatment. Further enrichment analyses indicated that ‘Up’ responders may resist treatment through reduced proliferation and increased interaction with the tumour microenvironment, whereas ‘Down’ responders instead rely on a shift to mesenchymal cell states. CONCLUSION These results indicate that GBM tumours can be split into two subtypes that transcriptionally reprogramme in different directions through treatment and may benefit from different treatment approaches.

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Park, Hee-Jung, Ju-Hye Choi, Myeong-Hyun Nam, and Young-Kwon Seo. "Induced Neurodifferentiation of hBM-MSCs through Activation of the ERK/CREB Pathway via Pulsed Electromagnetic Fields and Physical Stimulation Promotes Neurogenesis in Cerebral Ischemic Models." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1177. http://dx.doi.org/10.3390/ijms23031177.

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Stroke is among the leading causes of death worldwide, and stroke patients are more likely to live with permanent disabilities even after treatment. Several treatments are being developed to improve the quality of life of patients; however, these treatments still have important limitations. Our study thus sought to evaluate the neural differentiation of human bone marrow mesenchymal stem cells (hBM-MSCs) at various pulsed electromagnetic field (PEMF) frequencies. Furthermore, the effects of selected frequencies in vivo were also evaluated using a mouse ischemia stroke model. Cell proliferation decreased by 20% in the PEMF group, as demonstrated by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, and lactate dehydrogenase (LDH) secretion increased by approximately 10% in an LDH release assay. Fluorescence-activated cell sorting (FACS) analysis demonstrated that CD73 and CD105 were downregulated in the PEMF group at 60 Hz. Moreover, microtubule-associated protein 2 (MAP-2) and neurofilament light chain (NF-L) were upregulated in cell cultures at 60 and 75 Hz. To assess the effects of PEMF in vivo, cerebral ischemia mice were exposed to a PEMF at 60 Hz. Neural-related proteins were significantly upregulated in the PEMF groups compared with the control and cell group. Upon conducting rotarod tests, the cell/PEMF group exhibited significant differences in motor coordination at 13 days post-treatment when compared with the control and stem-cell-treated group. Furthermore, the cell and cell/PEMF group exhibited a significant reduction in the expression of matrix metalloproteinase-9 (MMP-9), tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) in the induced ischemic area compared with the control. Collectively, our findings demonstrated that PEMFs at 60 and 75 Hz could stimulate hBM-MSCs neural differentiation in vitro, in addition to promoting neurogenesis to enhance the functional recovery process by reducing the post-stroke inflammatory reaction.

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Kunzler, Alice, Fares Zeidán-Chuliá, Juciano Gasparotto, Carolina Saibro Girardi, Karina Klafke, Lyvia Lintzmaier Petiz, Rafael Calixto Bortolin, et al. "Changes in Cell Cycle and Up-Regulation of Neuronal Markers During SH-SY5Y Neurodifferentiation by Retinoic Acid are Mediated by Reactive Species Production and Oxidative Stress." Molecular Neurobiology 54, no. 9 (October 22, 2016): 6903–16. http://dx.doi.org/10.1007/s12035-016-0189-4.

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Slotkin, Theodore A., and Frederic J. Seidler. "Diverse neurotoxicants converge on gene expression for neuropeptides and their receptors in an in vitro model of neurodifferentiation: Effects of chlorpyrifos, diazinon, dieldrin and divalent nickel in PC12 cells." Brain Research 1353 (September 2010): 36–52. http://dx.doi.org/10.1016/j.brainres.2010.07.073.

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Urmann, Corinna, Eleni Oberbauer, Sébastien Couillard-Després, Ludwig Aigner, and Herbert Riepl. "Neurodifferentiating Potential of 8-Prenylnaringenin and Related Compounds in Neural Precursor Cells and Correlation with Estrogen-Like Activity." Planta Medica 81, no. 04 (February 25, 2015): 305–11. http://dx.doi.org/10.1055/s-0034-1396243.

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Bieluszewska, Anna, Phillip Wulfridge, John Doherty, Wenqing Ren, and Kavitha Sarma. "ATRX histone binding and helicase activities have distinct roles in neuronal differentiation." Nucleic Acids Research, August 24, 2022. http://dx.doi.org/10.1093/nar/gkac683.

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Abstract ATRX is a chromatin remodeler, which is mutated in ATRX syndrome, a neurodevelopmental disorder. ATRX mutations that alter histone binding or chromatin remodeling activities cluster in the PHD finger or the helicase domain respectively. Using engineered mouse embryonic stem cells that exclusively express ATRX protein with mutations in the PHD finger (PHDmut) or helicase domains (K1584R), we examine how specific ATRX mutations affect neurodifferentiation. ATRX PHDmut and K1584R proteins interact with the DAXX histone chaperone but show reduced localization to pericentromeres. Neurodifferentiation is both delayed and compromised in PHDmut and K1584R, and manifest differently from complete ATRX loss. We observe reduced enrichment of PHDmut protein to ATRX targets, while K1584R accumulates at these sites. Interestingly, ATRX mutations have distinct effects on the genome-wide localization of the polycomb repressive complex 2 (PRC2), with PHDmut and ATRX knockout showing reduced PRC2 binding at polycomb targets and K1584R showing loss at some sites and gains at others. Notably, each mutation associated with unique gene signatures, suggesting distinct pathways leading to impaired neurodifferentiation. Our results indicate that the histone binding and chromatin remodeling functions of ATRX play non-redundant roles in neurodevelopment, and when mutated lead to ATRX syndrome through separate regulatory pathways.

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