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Journal articles on the topic 'Neuronal differentiation'

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Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2023

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1

Kawaguchi, Tsutomu, Hiroaki Yokoyama, Masaru Inoue, Akio Ichikura, Masashige Onizuka, and Masao Kishikawa. "A Case of Pineocytoma with Neuronal Differentiation." Japanese Journal of Neurosurgery 4, no. 2 (1995): 180–84. http://dx.doi.org/10.7887/jcns.4.180.

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2

Léopold, Pierre. "Neuronal Differentiation." Cell 119, no. 1 (October 2004): 4–5. http://dx.doi.org/10.1016/j.cell.2004.09.024.

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3

Miyahara, Hiroaki, Manabu Natsumeda, Junichi Yoshimura, Yukihiko Fujii, Akiyoshi Kakita, Yasushi Iwasaki, and Mari Yoshida. "MBRS-32. TOPOISOMERASE II β INDUCES NEURONAL, BUT NOT GLIAL, DIFFERENTIATION IN MEDULLOBLASTOMA." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii404. http://dx.doi.org/10.1093/neuonc/noaa222.546.

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Abstract BACKGROUND We previously reported that Gli3, which was a downstream molecule of Sonic Hedgehog signal, induced neuronal and/or glial differentiation in some types of medulloblastoma (desmoplastic/nodular medulloblastoma and medulloblastoma with extensive nodularity), and patients of medulloblastoma with neuronal differentiation showed favorable prognosis, but those with glial differentiation tended to show miserable prognosis (Miyahara H, Neuropathology, 2013). This time, we focused on Topoisomerase II β (Top2β), which was reported to induce neuronal differentiation and inhibit glial differentiation, and examined the expression of Top2β in medulloblastomas with neuronal and glial differentiations. METHODS We assessed the expression of Top2β, NeuN, and GFAP using triple fluorescent immunostaining method in medulloblastoma samples with both neuronal and glial differentiations. Furthermore, the expression of Top2β, H3K4me2, and H3K27me3 were also assessed, because Top2βwas positively or negatively regulated by H3K4me2 and H3K27me3, respectively. RESULTS Many large nuclei in the nodules, in which differentiated cells were seen, was visualized by Top2β. The Top2β signals were seen in NeuN+ cells but not GFAP+ cells. H3K4me2 signals were visualized in Top2β+ large nuclei, but H3K27me3 and NeuN+ large nuclei were distributed independently. CONCLUSIONS These results indicate that Top2β may be a molecule associated with neuronal, but not glial, differentiation of medulloblastoma cells. Drugs targeting histone modification enzymes such as EZH2 inhibitors are possible therapeutic targets as a differentiation-inducing therapy for medulloblastoma.

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4

Pérez, María Julia, Tomas Roberto Carden, Paula Ayelen dos Santos Claro, Susana Silberstein, Pablo Martin Páez, Veronica Teresita Cheli, Jorge Correale, and Juana M. Pasquini. "Transferrin Enhances Neuronal Differentiation." ASN Neuro 15 (January 2023): 175909142311707. http://dx.doi.org/10.1177/17590914231170703.

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

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5

FUKUSHIMA, Takeo, Masamichi TOMONAGA, Toshio SAWADA, and Hiroshi IWASAKI. "Pineocytoma with Neuronal Differentiation." Neurologia medico-chirurgica 30, no. 1 (1990): 63–68. http://dx.doi.org/10.2176/nmc.30.63.

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6

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

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7

Rösner, H., M. Al-Aqtum, and H. Rahmann. "Gangliosides and neuronal differentiation." Neurochemistry International 20, no. 3 (April 1992): 339–51. http://dx.doi.org/10.1016/0197-0186(92)90048-v.

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8

Lamar, E., C. Kintner, and M. Goulding. "Identification of NKL, a novel Gli-Kruppel zinc-finger protein that promotes neuronal differentiation." Development 128, no. 8 (April 15, 2001): 1335–46. http://dx.doi.org/10.1242/dev.128.8.1335.

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The proneural basic helix-loop-helix proteins play a crucial role in promoting the differentiation of postmitotic neurons from neural precursors. However, recent evidence from flies and frogs indicates that additional factors act together with the proneural bHLH proteins to promote neurogenesis. We have identified a novel zinc finger protein, neuronal Kruppel-like protein (NKL), that positively regulates neurogenesis in vertebrates. NKL is expressed in Xenopus primary neurons and in differentiating neuronal precursors in the intermediate zone of the mouse and chick neural tube. In frog embryos, NKL is induced by overexpression of Neurogenin (Ngn), arguing that NKL is downstream of the proneural determination genes. Our results show that NKL and a NKL/VP16 fusion protein promote differentiation of neuronal precursors in the embryonic chick spinal cord. Following in ovo misexpression of NKL, neuroepithelial cells exit the cell cycle and differentiate into neurons. Similarly, NKL/VP16 induces extra primary neurons in frogs and upregulates expression of the neural differentiation factors, Xath3 and MyT1, as well as the neuronal markers, N-tubulin and elrC. Our findings establish NKL as a novel positive regulator of neuronal differentiation and provide further evidence that non-bHLH transcription factors function in the neuronal differentiation pathway activated by the vertebrate neuronal determination genes.

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9

Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, Stefan Putz, Kevin Achberger, Leonhard Linta, Stefan Liebau, Tobias M. Boeckers, and Andreas M. Grabrucker. "Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/3760702.

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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation.

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10

Erin, Nuray, and Özkan Ulusoy. "Differentiation of neuronal from non-neuronal Substance P." Regulatory Peptides 152, no. 1-3 (January 2009): 108–13. http://dx.doi.org/10.1016/j.regpep.2008.10.006.

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11

Chiu, Yi-Chi, Ming-Yang Li, Yuan-Hsuan Liu, Jing-Ya Ding, Jenn-Yah Yu, and Tsu-Wei Wang. "Foxp2 regulates neuronal differentiation and neuronal subtype specification." Developmental Neurobiology 74, no. 7 (February 18, 2014): 723–38. http://dx.doi.org/10.1002/dneu.22166.

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12

Lauter, Gilbert, Andrea Coschiera, Masahito Yoshihara, Debora Sugiaman-Trapman, Sini Ezer, Shalini Sethurathinam, Shintaro Katayama, Juha Kere, and Peter Swoboda. "Differentiation of ciliated human midbrain-derived LUHMES neurons." Journal of Cell Science 133, no. 21 (October 28, 2020): jcs249789. http://dx.doi.org/10.1242/jcs.249789.

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ABSTRACTMany human cell types are ciliated, including neural progenitors and differentiated neurons. Ciliopathies are characterized by defective cilia and comprise various disease states, including brain phenotypes, where the underlying biological pathways are largely unknown. Our understanding of neuronal cilia is rudimentary, and an easy-to-maintain, ciliated human neuronal cell model is absent. The Lund human mesencephalic (LUHMES) cell line is a ciliated neuronal cell line derived from human fetal mesencephalon. LUHMES cells can easily be maintained and differentiated into mature, functional neurons within one week. They have a single primary cilium as proliferating progenitor cells and as postmitotic, differentiating neurons. These developmental stages are completely separable within one day of culture condition change. The sonic hedgehog (SHH) signaling pathway is active in differentiating LUHMES neurons. RNA-sequencing timecourse analyses reveal molecular pathways and gene-regulatory networks critical for ciliogenesis and axon outgrowth at the interface between progenitor cell proliferation, polarization and neuronal differentiation. Gene expression dynamics of cultured LUHMES neurons faithfully mimic the corresponding in vivo dynamics of human fetal midbrain. In LUHMES cells, neuronal cilia biology can be investigated from proliferation through differentiation to mature neurons.

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13

Hisahara, Shin, Susumu Chiba, Hiroyuki Matsumoto, Masaya Tanno, Hideshi Yagi, Shun Shimohama, Makoto Sato, and Yoshiyuki Horio. "Histone deacetylase SIRT1 modulates neuronal differentiation by its nuclear translocation." Proceedings of the National Academy of Sciences 105, no. 40 (September 30, 2008): 15599–604. http://dx.doi.org/10.1073/pnas.0800612105.

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Neural precursor cells (NPCs) differentiate into neurons, astrocytes, and oligodendrocytes in response to intrinsic and extrinsic changes. Notch signals maintain undifferentiated NPCs, but the mechanisms underlying the neuronal differentiation are largely unknown. We show that SIRT1, an NAD+-dependent histone deacetylase, modulates neuronal differentiation. SIRT1 was found in the cytoplasm of embryonic and adult NPCs and was transiently localized in the nucleus in response to differentiation stimulus. SIRT1 started to translocate into the nucleus within 10 min after the transfer of NPCs into differentiation conditions, stayed in the nucleus, and then gradually retranslocated to the cytoplasm after several hours. The number of neurospheres that generated Tuj1+ neurons was significantly decreased by pharmacological inhibitors of SIRT1, dominant-negative SIRT1 and SIRT1-siRNA, whereas overexpression of SIRT1, but not that of cytoplasm-localized mutant SIRT1, enhanced neuronal differentiation and decreased Hes1 expression. Expression of SIRT1-siRNA impaired neuronal differentiation and migration of NPCs into the cortical plate in the embryonic brain. Nuclear receptor corepressor (N-CoR), which has been reported to bind SIRT1, promoted neuronal differentiation and synergistically increased the number of Tuj1+ neurons with SIRT1, and both bound the Hes1 promoter region in differentiating NPCs. Hes1 transactivation by Notch1 was inhibited by SIRT1 and/or N-CoR. Our study indicated that SIRT1 is a player of repressing Notch1-Hes1 signaling pathway, and its transient translocation into the nucleus may have a role in the differentiation of NPCs.

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14

Takeda, Yuji S., and Qiaobing Xu. "Neuronal Differentiation of Human Mesenchymal Stem Cells Using Exosomes Derived from Differentiating Neuronal Cells." PLOS ONE 10, no. 8 (August 6, 2015): e0135111. http://dx.doi.org/10.1371/journal.pone.0135111.

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15

Namsi, Amira, Thomas Nury, Haithem Hamdouni, Aline Yammine, Anne Vejux, Dominique Vervandier-Fasseur, Norbert Latruffe, Olfa Masmoudi-Kouki, and Gérard Lizard. "Induction of Neuronal Differentiation of Murine N2a Cells by Two Polyphenols Present in the Mediterranean Diet Mimicking Neurotrophins Activities: Resveratrol and Apigenin." Diseases 6, no. 3 (July 22, 2018): 67. http://dx.doi.org/10.3390/diseases6030067.

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In the prevention of neurodegeneration associated with aging and neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease), neuronal differentiation is of interest. In this context, neurotrophic factors are a family of peptides capable of promoting the growth, survival, and/or differentiation of both developing and immature neurons. In contrast to these peptidyl compounds, polyphenols are not degraded in the intestinal tract and are able to cross the blood–brain barrier. Consequently, they could potentially be used as therapeutic agents in neurodegenerative pathologies associated with neuronal loss, thus requiring the stimulation of neurogenesis. We therefore studied the ability to induce neuronal differentiation of two major polyphenols present in the Mediterranean diet: resveratrol (RSV), a major compound found in grapes and red wine, and apigenin (API), present in parsley, rosemary, olive oil, and honey. The effects of these compounds (RSV and API: 6.25–50 µM) were studied on murine neuro-2a (N2a) cells after 48 h of treatment without or with 10% fetal bovine serum (FBS). Retinoic acid (RA: 6.25–50 µM) was used as positive control. Neuronal differentiation was morphologically evaluated through the presence of dendrites and axons. Cell growth was determined by cell counting and cell viability by staining with fluorescein diacetate (FDA). Neuronal differentiation was more efficient in the absence of serum than with 10% FBS or 10% delipidized FBS. At concentrations inducing neuronal differentiation, no or slight cytotoxicity was observed with RSV and API, whereas RA was cytotoxic. Without FBS, RSV and API, as well as RA, trigger the neuronal differentiation of N2a cells via signaling pathways simultaneously involving protein kinase A (PKA)/phospholipase C (PLC)/protein kinase C (PKC) and MEK/ERK. With 10% FBS, RSV and RA induce neuronal differentiation via PLC/PKC and PKA/PLC/PKC, respectively. With 10% FBS, PKA and PLC/PKC as well as MEK/ERK signaling pathways were not activated in API-induced neuronal differentiation. In addition, the differentiating effects of RSV and API were not inhibited by cyclo[DLeu5] OP, an antagonist of octadecaneuropeptide (ODN) which is a neurotrophic factor. Moreover, RSV and API do not stimulate the expression of the diazepam-binding inhibitor (DBI), the precursor of ODN. Thus, RSV and API are able to induce neuronal differentiation, ODN and its receptor are not involved in this process, and the activation of the (PLC/PKC) signaling pathway is required, except with apigenin in the presence of 10% FBS. These data show that RSV and API are able to induce neuronal differentiation and therefore mimic neurotrophin activity. Thus, RSV and API could be of interest in regenerative medicine to favor neurogenesis.

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16

Patranabis, Somi, and Suvendra Nath Bhattacharyya. "Phosphorylation of Ago2 and Subsequent Inactivation of let-7a RNP-Specific MicroRNAs Control Differentiation of Mammalian Sympathetic Neurons." Molecular and Cellular Biology 36, no. 8 (February 8, 2016): 1260–71. http://dx.doi.org/10.1128/mcb.00054-16.

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MicroRNAs (miRNAs) are small regulatory RNAs that regulate gene expression posttranscriptionally by base pairing to the target mRNAs in animal cells.KRas, an oncogene known to be repressed by let-7a miRNAs, is expressed and needed for the differentiation of mammalian sympathetic neurons and PC12 cells. We documented a loss of let-7a activity during this differentiation process without any significant change in the cellular level of let-7a miRNA. However, the level of Ago2, an essential component that is associated with miRNAs to form RNP-specific miRNA (miRNP) complexes, shows an increase with neuronal differentiation. In this study, differentiation-induced phosphorylation and the subsequent loss of miRNA from Ago2 were noted, and these accounted for the loss of miRNA activity in differentiating neurons. Neuronal differentiation induces the phosphorylation of mitogen-activated protein kinase p38 and the downstream kinase mitogen- and stress-activated protein kinase 1 (MSK1). This in turn upregulates the phosphorylation of Ago2 and ensures the dissociation of miRNA from Ago2 in neuronal cells. MSK1-mediated miRNP inactivation is a prerequisite for the differentiation of neuronal cells, where let-7a miRNA gets unloaded from Ago2 to ensure the upregulation ofKRas, a target of let-7a. We noted that the inactivation of let-7a is both necessary and sufficient for the differentiation of sympathetic neurons.

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17

Villalta, Jimmy, and Karin B. Busch. "Mitochondrial heterogeneity during neuronal differentiation." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1863 (September 2022): 148886. http://dx.doi.org/10.1016/j.bbabio.2022.148886.

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18

Agostini, M., F. Romeo, S. Inoue, M. V. Niklison-Chirou, A. J. Elia, D. Dinsdale, N. Morone, R. A. Knight, T. W. Mak, and G. Melino. "Metabolic reprogramming during neuronal differentiation." Cell Death & Differentiation 23, no. 9 (April 8, 2016): 1502–14. http://dx.doi.org/10.1038/cdd.2016.36.

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19

Park, Chul-Kee, Ji Hoon Phi, and Sung-Hye Park. "Glial Tumors with Neuronal Differentiation." Neurosurgery Clinics of North America 26, no. 1 (January 2015): 117–38. http://dx.doi.org/10.1016/j.nec.2014.09.006.

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20

Chisholm, Andrew D., and Yishi Jin. "Neuronal differentiation in C. elegans." Current Opinion in Cell Biology 17, no. 6 (December 2005): 682–89. http://dx.doi.org/10.1016/j.ceb.2005.10.004.

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21

Burgoyne, Robert D. "Microtubule proteins in neuronal differentiation." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 83, no. 1 (January 1986): 1–8. http://dx.doi.org/10.1016/0305-0491(86)90323-8.

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22

Zhao, Fei, Tongde Wu, Alexandria Lau, Tao Jiang, Zheping Huang, Xiao-Jun Wang, Weimin Chen, Pak Kin Wong, and Donna D. Zhang. "Nrf2 promotes neuronal cell differentiation." Free Radical Biology and Medicine 47, no. 6 (September 2009): 867–79. http://dx.doi.org/10.1016/j.freeradbiomed.2009.06.029.

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23

Naujok, Ortwin, Flavio Francini, Sally Picton, Anne Jörns, Clifford J. Bailey, and Sigurd Lenzen. "A New Experimental Protocol for Preferential Differentiation of Mouse Embryonic Stem Cells into Insulin-Producing Cells." Cell Transplantation 17, no. 10-11 (October 2008): 1231–42. http://dx.doi.org/10.3727/096368908787236549.

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Mouse embryonic stem (ES) cells have the potential to differentiate into insulin-producing cells, but efficient protocols for in vitro differentiation have not been established. Here we have developed a new optimized four-stage differentiation protocol and compared this with an established reference protocol. The new protocol minimized differentiation towards neuronal progeny, resulting in a population of insulin-producing cells with β-cell characteristics but lacking neuronal features. The yield of glucagon and somatostatin cells was negligible. Crucial for this improved yield was the removal of a nestin selection step as well as removal of culture supplements that promote differentiation towards the neuronal lineage. Supplementation of the differentiation medium with insulin and fetal calf serum was beneficial for differentiation towards monohormonal insulin-positive cells. After implantation into diabetic mice these insulin-producing cells produced a time-dependent improvement of the diabetic metabolic state, in contrast to cells differentiated according to the reference protocol. Using a spinner culture instead of an adherent culture of ES cells prevented the differentiation towards insulin-producing cells. Thus, prevention of cell attachment in a spinner culture represents a means to keep ES cells in an undifferentiated state and to inhibit differentiation. In conclusion, this study describes a new optimized four-stage protocol for differentiating ES cells to insulin-producing cells with minimal neuronal cell formation.

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24

Ogura, Tsutomu, Kohzo Nakayama, Hironori Fujisawa, and Hiroyasu Esumi. "Neuronal nitric oxide synthase expression in neuronal cell differentiation." Neuroscience Letters 204, no. 1-2 (February 1996): 89–92. http://dx.doi.org/10.1016/0304-3940(96)12324-7.

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25

Papalopulu, N., and C. Kintner. "A posteriorising factor, retinoic acid, reveals that anteroposterior patterning controls the timing of neuronal differentiation in Xenopus neuroectoderm." Development 122, no. 11 (November 1, 1996): 3409–18. http://dx.doi.org/10.1242/dev.122.11.3409.

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During early development of the Xenopus central nervous system (CNS), neuronal differentiation can be detected posteriorly at neural plate stages but is delayed anteriorly until after neural tube closure. A similar delay in neuronal differentiation also occurs in the anterior neural tissue that forms in vitro when isolated ectoderm is treated with the neural inducer noggin. Here we examine the factors that control the timing of neuronal differentiation both in embryos and in neural tissue induced by noggin (noggin caps). We show that the delay in neuronal differentiation that occurs in noggin caps cannot be overcome by inhibiting the activity of the neurogenic gene, X-Delta-1, which normally inhibits neuronal differentiation, suggesting that it represents a novel level of regulation. Conversely, we show that the timing of neuronal differentiation can be changed from late to early after treating noggin caps or embryos with retinoic acid (RA), a putative posteriorising agent. Concommittal with changes in the timing of neuronal differentiation, RA suppresses the expression of anterior neural genes and promotes the expression of posterior neural genes. The level of early neuronal differentiation induced by RA alone is greatly increased by the additional expression of the proneural gene, XASH3. These results indicate that early neuronal differentiation in neuralised ectoderm requires posteriorising signals, as well as signals that promote the activity of proneural genes such as XASH3. In addition, these result suggest that neuronal differentiation is controlled by anteroposterior (A-P) patterning, which exerts a temporal control on the onset of neuronal differentiation.

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Zhang, Jin, and Xinbin Chen. "ΔNp73 Modulates Nerve Growth Factor-Mediated Neuronal Differentiation through Repression of TrkA." Molecular and Cellular Biology 27, no. 10 (March 12, 2007): 3868–80. http://dx.doi.org/10.1128/mcb.02112-06.

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ABSTRACT p73, a member of the p53 family, expresses two classes of proteins: the full-length TAp73 and the N-terminally truncated ΔNp73. While TAp73 possesses many p53-like features, ΔNp73 is dominant negative towards TAp73 and p53 and appears to have distinct functions in tumorigenesis and neuronal development. Given its biological importance, we investigated the role of ΔNp73 in nerve growth factor (NGF)-mediated neuronal differentiation in PC12 cells. We show that overexpression of ΔNp73α or ΔNp73β inhibits NGF-mediated neuronal differentiation in both p53-dependent and -independent manners. In line with this, we showed that the level of endogenous ΔNp73 is progressively diminished in differentiating PC12 cells upon NGF treatment and knockdown of ΔNp73 promotes NGF-mediated neuronal differentiation. Interestingly, we found that the ability of ΔNp73 to suppress NGF-mediated neuronal differentiation is correlated with its ability to regulate the expression of TrkA, the high-affinity NGF receptor. Specifically, we found that ΔNp73 directly binds to the TrkA promoter and transcriptionally represses TrkA expression, which in turn attenuates the NGF-mediated mitogen-activated protein kinase pathway. Conversely, the steady-state level of TrkA is increased upon knockdown of ΔNp73. Furthermore, we found that histone deacetylase 1 (HDAC1) and HDAC2 are recruited by ΔNp73 to the TrkA promoter and act as corepressors to suppress TrkA expression, which can be relieved by trichostatin A, an HDAC inhibitor. Taken together, we conclude that ΔNp73 negatively regulates NGF-mediated neuronal differentiation by transrepressing TrkA.

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Hernández, Rosa, Cristina Jiménez-Luna, Raúl Ortiz, Fernando Setién, Miguel López, Gloria Perazzoli, Manel Esteller, María Berdasco, Jose Prados, and Consolación Melguizo. "Impact of the Epigenetically Regulated Hoxa-5 Gene in Neural Differentiation from Human Adipose-Derived Stem Cells." Biology 10, no. 8 (August 19, 2021): 802. http://dx.doi.org/10.3390/biology10080802.

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Human adipose-derived mesenchymal stem cells (hASCs) may be used in some nervous system pathologies, although obtaining an adequate degree of neuronal differentiation is an important barrier to their applicability. This requires a deep understanding of the expression and epigenetic changes of the most important genes involved in their differentiation. We used hASCs from human lipoaspirates to induce neuronal-like cells through three protocols (Neu1, 2, and 3), determined the degree of neuronal differentiation using specific biomarkers in culture cells and neurospheres, and analyzed epigenetic changes of genes involved in this differentiation. Furthermore, we selected the Hoxa-5 gene to determine its potential to improve neuronal differentiation. Our results showed that an excellent hASC neuronal differentiation process using Neu1 which efficiently modulated NES, CHAT, SNAP25, or SCN9A neuronal marker expression. In addition, epigenetic studies showed relevant changes in Hoxa-5, GRM4, FGFR1, RTEL1, METRN, and PAX9 genes. Functional studies of the Hoxa-5 gene using CRISPR/dCas9 and lentiviral systems showed that its overexpression induced hASCs neuronal differentiation that was accelerated with the exposure to Neu1. These results suggest that Hoxa-5 is an essential gene in hASCs neuronal differentiation and therefore, a potential candidate for the development of cell therapy strategies in neurological disorders.

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Valeri, Andrea, Luigi Chiricosta, Simone D’Angiolini, Federica Pollastro, Stefano Salamone, and Emanuela Mazzon. "Cannabichromene Induces Neuronal Differentiation in NSC-34 Cells: Insights from Transcriptomic Analysis." Life 13, no. 3 (March 9, 2023): 742. http://dx.doi.org/10.3390/life13030742.

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Phytocannabinoids, with their variety of beneficial effects, represent a valid group of substances that could be employed as neurogenesis-enhancers or neuronal differentiation inducers. We focused our attention on the neuronal-related potential of cannabichromene (CBC) when administered to undifferentiated NSC-34 for 24 h. Transcriptomic analysis showed an upregulation of several neuronal markers, such as Neurod1 and Tubb3, as well as indicators of neuronal differentiation process progression, such as Pax6. An in-depth investigation of the processes involved in neuronal differentiation indicates positive cytoskeleton remodeling by upregulation of Cfl2 and Tubg1, and active differentiation-targeted transcriptional program, suggested by Phox2b and Hes1. After 48 h of treatment, the markers previously examined in the transcriptomic analysis are still overexpressed, like Ache and Hes1, indicating that the differentiation process is still in progress. The lack of GFAP protein suggests that no astroglial differentiation is taking place, and it is reasonable to indicate the neuronal one as the ongoing one. These results indicate CBC as a potential neuronal differentiation inducer for NSC-34 cells.

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29

Poluha, W., D. K. Poluha, B. Chang, N. E. Crosbie, C. M. Schonhoff, D. L. Kilpatrick, and A. H. Ross. "The cyclin-dependent kinase inhibitor p21 (WAF1) is required for survival of differentiating neuroblastoma cells." Molecular and Cellular Biology 16, no. 4 (April 1996): 1335–41. http://dx.doi.org/10.1128/mcb.16.4.1335.

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We are employing recent advances in the understanding of the cell cycle to study the inverse relationship between proliferation and neuronal differentiation. Nerve growth factor and aphidicolin, an inhibitor of DNA polymerases, synergistically induce neuronal differentiation of SH-SY5Y neuroblastoma cells and the expression of p21WAF1, an inhibitor of cyclin-dependent kinases. The differentiated cells continue to express p21WAF1, even after removal of aphidicolin from the culture medium. The p21WAF1 protein coimmunoprecipitates with cyclin E and inhibits cyclin E-associated protein kinase activity. Each of three antisense oligonucleotides complementary to p21WAF1 mRNA partially blocks expression of p21WAF1 and promotes programmed cell death. These data indicate that p21WAF1 expression is required for survival of these differentiating neuroblastoma cells. Thus, the problem of neuronal differentiation can now be understood in the context of negative regulators of the cell cycle.

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30

Wang, Feifei, Joseph J. Tidei, Eric D. Polich, Yu Gao, Huashan Zhao, Nora I. Perrone-Bizzozero, Weixiang Guo, and Xinyu Zhao. "Positive feedback between RNA-binding protein HuD and transcription factor SATB1 promotes neurogenesis." Proceedings of the National Academy of Sciences 112, no. 36 (August 24, 2015): E4995—E5004. http://dx.doi.org/10.1073/pnas.1513780112.

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The mammalian embryonic lethal abnormal vision (ELAV)-like protein HuD is a neuronal RNA-binding protein implicated in neuronal development, plasticity, and diseases. Although HuD has long been associated with neuronal development, the functions of HuD in neural stem cell differentiation and the underlying mechanisms have gone largely unexplored. Here we show that HuD promotes neuronal differentiation of neural stem/progenitor cells (NSCs) in the adult subventricular zone by stabilizing the mRNA of special adenine–thymine (AT)-rich DNA-binding protein 1 (SATB1), a critical transcriptional regulator in neurodevelopment. We find that SATB1 deficiency impairs the neuronal differentiation of NSCs, whereas SATB1 overexpression rescues the neuronal differentiation phenotypes resulting from HuD deficiency. Interestingly, we also discover that SATB1 is a transcriptional activator of HuD during NSC neuronal differentiation. In addition, we demonstrate that NeuroD1, a neuronal master regulator, is a direct downstream target of SATB1. Therefore, HuD and SATB1 form a positive regulatory loop that enhances NeuroD1 transcription and subsequent neuronal differentiation. Our results here reveal a novel positive feedback network between an RNA-binding protein and a transcription factor that plays critical regulatory roles in neurogenesis.

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Attia, Mikaël, Christophe Rachez, Antoine De Pauw, Philip Avner, and Ute Christine Rogner. "Nap1l2 Promotes Histone Acetylation Activity during Neuronal Differentiation." Molecular and Cellular Biology 27, no. 17 (June 25, 2007): 6093–102. http://dx.doi.org/10.1128/mcb.00789-07.

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ABSTRACT The deletion of the neuronal Nap1l2 (nucleosome assembly protein 1-like 2) gene in mice causes neural tube defects. We demonstrate here that this phenotype correlates with deficiencies in differentiation and increased maintenance of the neural stem cell stage. Nap1l2 associates with chromatin and interacts with histones H3 and H4. Loss of Nap1l2 results in decreased histone acetylation activity, leading to transcriptional changes in differentiating neurons, which include the marked downregulation of the Cdkn1c (cyclin-dependent kinase inhibitor 1c) gene. Cdkn1c expression normally increases during neuronal differentiation, and this correlates with the specific recruitment of the Nap1l2 protein and an increase in acetylated histone H3K9/14 at the site of Cdkn1c transcription. These results lead us to suggest that the Nap1l2 protein plays an important role in regulating transcription in developing neurons via the control of histone acetylation. Our data support the idea that neuronal nucleosome assembly proteins mediate cell-type-specific mechanisms of establishment/modification of a chromatin-permissive state that can affect neurogenesis and neuronal survival.

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Iglesias, Eldris, M. Pilar Bayona-Bafaluy, Alba Pesini, Nuria Garrido-Pérez, Patricia Meade, Paula Gaudó, Irene Jiménez-Salvador, Julio Montoya, and Eduardo Ruiz-Pesini. "Uridine Prevents Negative Effects of OXPHOS Xenobiotics on Dopaminergic Neuronal Differentiation." Cells 8, no. 11 (November 8, 2019): 1407. http://dx.doi.org/10.3390/cells8111407.

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Neuronal differentiation appears to be dependent on oxidative phosphorylation capacity. Several drugs inhibit oxidative phosphorylation and might be detrimental for neuronal differentiation. Some pregnant women take these medications during their first weeks of gestation when fetal nervous system is being developed. These treatments might have later negative consequences on the offspring’s health. To analyze a potential negative effect of three widely used medications, we studied in vitro dopaminergic neuronal differentiation of cells exposed to pharmacologic concentrations of azidothymidine for acquired immune deficiency syndrome; linezolid for multidrug-resistant tuberculosis; and atovaquone for malaria. We also analyzed the dopaminergic neuronal differentiation in brains of fetuses from pregnant mice exposed to linezolid. The drugs reduced the in vitro oxidative phosphorylation capacity and dopaminergic neuronal differentiation. This differentiation process does not appear to be affected in the prenatally exposed fetus brain. Nevertheless, the global DNA methylation in fetal brain was significantly altered, perhaps linking an early exposure to a negative effect in older life. Uridine was able to prevent the negative effects on in vitro dopaminergic neuronal differentiation and on in vivo global DNA methylation. Uridine could be used as a protective agent against oxidative phosphorylation-inhibiting pharmaceuticals provided during pregnancy when dopaminergic neuronal differentiation is taking place.

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Morelli, Sabrina, Antonella Piscioneri, Enrico Drioli, and Loredana De Bartolo. "Neuronal Differentiation Modulated by Polymeric Membrane Properties." Cells Tissues Organs 204, no. 3-4 (2017): 164–78. http://dx.doi.org/10.1159/000477135.

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In this study, different collagen-blend membranes were successfully constructed by blending collagen with chitosan (CHT) or poly(lactic-co-glycolic acid) (PLGA) to enhance their properties and thus create new biofunctional materials with great potential use for neuronal tissue engineering and regeneration. Collagen blending strongly affected membrane properties in the following ways: (i) it improved the surface hydrophilicity of both pure CHT and PLGA membranes, (ii) it reduced the stiffness of CHT membranes, but (iii) it did not modify the good mechanical properties of PLGA membranes. Then, we investigated the effect of the different collagen concentrations on the neuronal behavior of the membranes developed. Morphological observations, immunocytochemistry, and morphometric measures demonstrated that the membranes developed, especially CHT/Col30, PLGA, and PLGA/Col1, provided suitable microenvironments for neuronal growth owing to their enhanced properties. The most consistent neuronal differentiation was obtained in neurons cultured on PLGA-based membranes, where a well-developed neuronal network was achieved due to their improved mechanical properties. Our findings suggest that tensile strength and elongation at break are key material parameters that have potential influence on both axonal elongation and neuronal structure and organization, which are of fundamental importance for the maintenance of efficient neuronal growth. Hence, our study has provided new insights regarding the effects of membrane mechanical properties on neuronal behavior, and thus it may help to design and improve novel instructive biomaterials for neuronal tissue engineering.

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Ehrhart-Bornstein, M., V. Vukicevic, K. F. Chung, and S. R. Bornstein. "Neuronal differentiation of chromaffin progenitor cells." Molecular Psychiatry 14, no. 1 (December 19, 2008): 1. http://dx.doi.org/10.1038/mp.2008.129.

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35

Johnson, Dianna A., Jiakun Zhang, Sharon Frase, Matthew Wilson, Carlos Rodriguez-Galindo, and Michael A. Dyer. "Neuronal Differentiation and Synaptogenesis in Retinoblastoma." Cancer Research 67, no. 6 (March 15, 2007): 2701–11. http://dx.doi.org/10.1158/0008-5472.can-06-3754.

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36

Garcia-Gutierrez, P., F. Juarez-Vicente, D. J. Wolgemuth, and M. Garcia-Dominguez. "Pleiotrophin antagonizes Brd2 during neuronal differentiation." Journal of Cell Science 127, no. 11 (April 2, 2014): 2554–64. http://dx.doi.org/10.1242/jcs.147462.

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37

Mak, Nai-Ki, Wen-Kui Li, Meng Zhang, Ricky Ngok-Shun Wong, Lai-Shan Tai, Ken Kin-Lam Yung, and Hi-Wun Leung. "Effects of euxanthone on neuronal differentiation." Life Sciences 66, no. 4 (December 1999): 347–54. http://dx.doi.org/10.1016/s0024-3205(99)00596-2.

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38

Thompson, Alex F., and Leonard A. Levin. "Neuronal differentiation by analogs of staurosporine." Neurochemistry International 56, no. 4 (March 2010): 554–60. http://dx.doi.org/10.1016/j.neuint.2009.12.018.

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39

Matas-Rico, Elisa, Michiel van Veen, and Wouter H. Moolenaar. "Neuronal differentiation through GPI-anchor cleavage." Cell Cycle 16, no. 5 (March 4, 2017): 388–89. http://dx.doi.org/10.1080/15384101.2016.1259894.

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40

Bignami, F., P. Bevilacqua, S. Biagioni, A. De Jaco, F. Casamenti, A. Felsani, and G. Augusti-Tocco. "Cellular Acetylcholine Content and Neuronal Differentiation." Journal of Neurochemistry 69, no. 4 (October 1997): 1374–81. http://dx.doi.org/10.1046/j.1471-4159.1997.69041374.x.

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41

Janesick, Amanda, Stephanie Cherie Wu, and Bruce Blumberg. "Retinoic acid signaling and neuronal differentiation." Cellular and Molecular Life Sciences 72, no. 8 (January 6, 2015): 1559–76. http://dx.doi.org/10.1007/s00018-014-1815-9.

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42

van Inzen, Wouter G., Maikel P. Peppelenbosch, Maria W. M. van den Brand, Leon G. J. Tertoolen, and Siegfried W. de Laat. "Neuronal differentiation of embryonic stem cells." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1312, no. 1 (June 1996): 21–26. http://dx.doi.org/10.1016/0167-4889(96)00011-0.

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43

Morrison, Sean J. "Neuronal differentiation: Proneural genes inhibit gliogenesis." Current Biology 11, no. 9 (May 2001): R349—R351. http://dx.doi.org/10.1016/s0960-9822(01)00191-9.

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Garcia-Dominguez, Mario, and Pablo Garcia-Gutierrez. "Pleiotrophin fights Brd2 for neuronal differentiation." Neural Regeneration Research 10, no. 4 (2015): 544. http://dx.doi.org/10.4103/1673-5374.155416.

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OBERMEIER, AXEL, RALPH A. BRADSHAW, KLAUS SEEDORF, AXEL CHOIDAS, JOSEPH SCHLESSINGER, and AXEL ULLRICH. "Definition of Signals for Neuronal Differentiation." Annals of the New York Academy of Sciences 766, no. 1 Receptor Acti (September 1995): 1–17. http://dx.doi.org/10.1111/j.1749-6632.1995.tb26643.x.

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46

Novitch, Bennett G., and Samantha J. Butler. "Reducing the Mystery of Neuronal Differentiation." Cell 138, no. 6 (September 2009): 1062–64. http://dx.doi.org/10.1016/j.cell.2009.09.001.

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47

Tomlinson, Andrew, and Donald F. Ready. "Neuronal differentiation in the Drosophila ommatidium." Developmental Biology 120, no. 2 (April 1987): 366–76. http://dx.doi.org/10.1016/0012-1606(87)90239-9.

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48

Keegan, Kathleen, and Simon Halegoua. "Signal transduction pathways in neuronal differentiation." Current Opinion in Neurobiology 3, no. 1 (February 1993): 14–19. http://dx.doi.org/10.1016/0959-4388(93)90029-x.

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49

Verdile, Veronica, Francesca Svetoni, Piergiorgio La Rosa, Gabriele Ferrante, Eleonora Cesari, Claudio Sette, and Maria Paola Paronetto. "EWS splicing regulation contributes to balancing Foxp1 isoforms required for neuronal differentiation." Nucleic Acids Research 50, no. 6 (March 7, 2022): 3362–78. http://dx.doi.org/10.1093/nar/gkac154.

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Abstract Alternative splicing is a key regulatory process underlying the amplification of genomic information and the expansion of proteomic diversity, particularly in brain. Here, we identify the Ewing sarcoma protein (EWS) as a new player of alternative splicing regulation during neuronal differentiation. Knockdown of EWS in neuronal progenitor cells leads to premature differentiation. Transcriptome profiling of EWS-depleted cells revealed global changes in splicing regulation. Bioinformatic analyses and biochemical experiments demonstrated that EWS regulates alternative exons in a position-dependent fashion. Notably, several EWS-regulated splicing events are physiologically modulated during neuronal differentiation and EWS depletion in neuronal precursors anticipates the splicing-pattern of mature neurons. Among other targets, we found that EWS controls the alternative splicing of the forkhead family transcription factor FOXP1, a pivotal transcriptional regulator of neuronal differentiation, possibly contributing to the switch of gene expression underlying the neuronal differentiation program.

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50

Gershon, A. A., J. Rudnick, L. Kalam, and K. Zimmerman. "The homeodomain-containing gene Xdbx inhibits neuronal differentiation in the developing embryo." Development 127, no. 13 (July 1, 2000): 2945–54. http://dx.doi.org/10.1242/dev.127.13.2945.

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The development of the vertebrate nervous system depends upon striking a balance between differentiating neurons and neural progenitors in the early embryo. Our findings suggest that the homeodomain-containing gene Xdbx regulates this balance by maintaining neural progenitor populations within specific regions of the neuroectoderm. In posterior regions of the Xenopus embryo, Xdbx is expressed in a bilaterally symmetric stripe that lies at the middle of the mediolateral axis of the neural plate. This stripe of Xdbx expression overlaps the expression domain of the proneural basic/helix-loop-helix-containing gene, Xash3, and is juxtaposed to the expression domains of Xenopus Neurogenin related 1 and N-tubulin, markers of early neurogenesis in the embryo. Xdbx overexpression inhibits neuronal differentiation in the embryo and when co-injected with Xash3, Xdbx inhibits the ability of Xash3 to induce ectopic neurogenesis. One role of Xdbx during normal development may therefore be to restrict spatially neuronal differentiation within the neural plate, possibly by altering the neuronal differentiation function of Xash3.

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