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Journal articles on the topic 'NSC-34'

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Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Nango, Hiroshi, Yasuhiro Kosuge, Masaki Sato, Yoshiyuki Shibukawa, Yuri Aono, Tadashi Saigusa, Yoshihisa Ito, and Kumiko Ishige. "Highly Efficient Conversion of Motor Neuron-Like NSC-34 Cells into Functional Motor Neurons by Prostaglandin E2." Cells 9, no. 7 (July 21, 2020): 1741. http://dx.doi.org/10.3390/cells9071741.

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Motor neuron diseases are a group of progressive neurological disorders that degenerate motor neurons. The neuroblastoma × spinal cord hybrid cell line NSC-34 is widely used as an experimental model in studies of motor neuron diseases. However, the differentiation efficiency of NSC-34 cells to neurons is not always sufficient. We have found that prostaglandin E2 (PGE2) induces morphological differentiation in NSC-34 cells. The present study investigated the functional properties of PGE2-differentiated NSC-34 cells. Retinoic acid (RA), a widely-used agent inducing cell differentiation, facilitated neuritogenesis, which peaked on day 7, whereas PGE2-induced neuritogenesis took only 2 days to reach the same level. Whole-cell patch-clamp recordings showed that the current threshold of PGE2-treated cell action potentials was lower than that of RA-treated cells. PGE2 and RA increased the protein expression levels of neuronal differentiation markers, microtubule-associated protein 2c and synaptophysin, and to the same extent, motor neuron-specific markers HB9 and Islet-1. On the other hand, protein levels of choline acetyltransferase and basal release of acetylcholine in PGE2-treated cells were higher than in RA-treated cells. These results suggest that PGE2 is a rapid and efficient differentiation-inducing factor for the preparation of functionally mature motor neurons from NSC-34 cells.

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2

Gyawali, Asmita, and Young-Sook Kang. "Pretreatment Effect of Inflammatory Stimuli and Characteristics of Tryptophan Transport on Brain Capillary Endothelial (TR-BBB) and Motor Neuron Like (NSC-34) Cell Lines." Biomedicines 9, no. 1 (December 24, 2020): 9. http://dx.doi.org/10.3390/biomedicines9010009.

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Tryptophan plays a key role in several neurological and psychiatric disorders. In this study, we investigated the transport mechanisms of tryptophan in brain capillary endothelial (TR-BBB) cell lines and motor neuron-like (NSC-34) cell lines. The uptake of [3H]l-tryptophan was stereospecific, and concentration- and sodium-dependent in TR-BBB cell lines. Transporter inhibitors and several neuroprotective drugs inhibited [3H]l-tryptophan uptake by TR-BBB cell lines. Gabapentin and baclofen exerted a competitive inhibitory effect on [3H]l-tryptophan uptake. Additionally, l-tryptophan uptake was time- and concentration-dependent in both NSC-34 wild type (WT) and mutant type (MT) cell lines, with a lower transporter affinity and higher capacity in MT than in WT cell lines. Gene knockdown of LAT1 (l-type amino acid transporter 1) and CAT1 (cationic amino acid transporter 1) demonstrated that LAT1 is primarily involved in the transport of [3H]l-tryptophan in both TR-BBB and NSC-34 cell lines. In addition, tryptophan uptake was increased by TR-BBB cell lines but decreased by NSC-34 cell lines after pro-inflammatory cytokine pre-treatment. However, treatment with neuroprotective drugs ameliorated tryptophan uptake by NSC-34 cell lines after inflammatory cytokines pretreatment. The tryptophan transport system may provide a therapeutic target for treating or preventing neurodegenerative diseases.

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3

Gyawali, Asmita, Seung Jae Hyeon, Hoon Ryu, and Young-Sook Kang. "The Alteration of L-Carnitine Transport and Pretreatment Effect under Glutamate Cytotoxicity on Motor Neuron-Like NSC-34 Lines." Pharmaceutics 13, no. 4 (April 14, 2021): 551. http://dx.doi.org/10.3390/pharmaceutics13040551.

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L-Carnitine (LC) is essential for transporting fatty acids to the mitochondria for β-oxidation. This study was performed to examine the alteration of the LC transport system in wild type (WT, NSC-34/hSOD1WT) and mutant type (MT, NSC-34/hSOD1G93A) amyotrophic lateral sclerosis (ALS) models. The uptake of [3H]L-carnitine was dependent on time, temperature, concentration, sodium, pH, and energy in both cell lines. The Michaelis–Menten constant (Km) value as well as maximum transport velocity (Vmax) indicated that the MT cell lines showed the higher affinity and lower capacity transport system, compared to that of the WT cell lines. Additionally, LC uptake was inhibited by organic cationic compounds but unaffected by organic anions. OCTN1/slc22a4 and OCTN2/slc22a5 siRNA transfection study revealed both transporters are involved in LC transport in NSC-34 cell lines. Additionally, slc22a4 and slc22a5 was significantly decreased in mouse MT models compared with that in ALS WT littermate models in the immune-reactivity study. [3H]L-Carnitine uptake and mRNA expression pattern showed the pretreatment of LC and acetyl L-carnitine (ALC) attenuated glutamate induced neurotoxicity in NSC-34 cell lines. These findings indicate that LC and ALC supplementation can prevent the neurotoxicity and neuro-inflammation induced by glutamate in motor neurons.

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4

Kosuge, Yasuhiro, Hiroshi Nango, Hiroki Kasai, Takuya Yanagi, Takayuki Mawatari, Kenta Nishiyama, Hiroko Miyagishi, Kumiko Ishige, and Yoshihisa Ito. "Generation of Cellular Reactive Oxygen Species by Activation of the EP2 Receptor Contributes to Prostaglandin E2-Induced Cytotoxicity in Motor Neuron-Like NSC-34 Cells." Oxidative Medicine and Cellular Longevity 2020 (January 11, 2020): 1–14. http://dx.doi.org/10.1155/2020/6101838.

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Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease characterized by progressive degeneration of motor neurons in the central nervous system. Prostaglandin E2 (PGE2) plays a pivotal role in the degeneration of motor neurons in human and transgenic models of ALS. We have shown previously that PGE2 directly induces neuronal death through activation of the E-prostanoid (EP) 2 receptor in differentiated NSC-34 cells, a motor neuron-like cell line. In the present study, to clarify the mechanisms underlying PGE2-induced neurotoxicity, we focused on generation of intracellular reactive oxygen species (ROS) and examined the effects of N-acetylcysteine (NAC), a cell-permeable antioxidant, on PGE2-induced cell death in differentiated NSC-34 cells. Dichlorofluorescein (DCF) fluorescence analysis of PGE2-treated cells showed that intracellular ROS levels increased markedly with time, and that this effect was antagonized by a selective EP2 antagonist (PF-04418948) but not a selective EP3 antagonist (L-798,106). Although an EP2-selective agonist, butaprost, mimicked the effect of PGE2, an EP1/EP3 agonist, sulprostone, transiently but significantly decreased the level of intracellular ROS in these cells. MTT reduction assay and lactate dehydrogenase release assay revealed that PGE2- and butaprost-induced cell death were each suppressed by pretreatment with NAC in a concentration-dependent manner. Western blot analysis revealed that the active form of caspase-3 was markedly increased in the PGE2- and butaprost-treated cells. These increases in caspase-3 protein expression were suppressed by pretreatment with NAC. Moreover, dibutyryl-cAMP treatment of differentiated NSC-34 cells caused intracellular ROS generation and cell death. Our data reveal the existence of a PGE2-EP2 signaling-dependent intracellular ROS generation pathway, with subsequent activation of the caspase-3 cascade, in differentiated NSC-34 cells, suggesting that PGE2 is likely a key molecule linking inflammation to oxidative stress in motor neuron-like NSC-34 cells.

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5

Keilhoff, Gerburg, Benjamin Lucas, Josephine Pinkernelle, Michael Steiner, and Hisham Fansa. "Effects of cerebrolysin on motor-neuron-like NSC-34 cells." Experimental Cell Research 327, no. 2 (October 2014): 234–55. http://dx.doi.org/10.1016/j.yexcr.2014.06.020.

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6

Kanjilal, Baishali, Brian M. Keyser, Devon K. Andres, Eric Nealley, Betty Benton, Ashley A. Melber, Jaclynn F. Andres, Valerie A. Letukas, Offie Clark, and Radharaman Ray. "Differentiated NSC-34 cells as anin vitrocell model for VX." Toxicology Mechanisms and Methods 24, no. 7 (September 11, 2014): 488–94. http://dx.doi.org/10.3109/15376516.2014.943442.

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7

Sabitha, K. R., D. Sanjay, B. Savita, T. R. Raju, and T. R. Laxmi. "Electrophysiological characterization of Nsc-34 cell line using Microelectrode Array." Journal of the Neurological Sciences 370 (November 2016): 134–39. http://dx.doi.org/10.1016/j.jns.2016.09.038.

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8

Gill, Anna L., Monica Z. Wang, Beth Levine, Alan Premasiri, and Fernando G. Vieira. "Primary Neurons and Differentiated NSC-34 Cells Are More Susceptible to Arginine-Rich ALS Dipeptide Repeat Protein-Associated Toxicity than Non-Differentiated NSC-34 and CHO Cells." International Journal of Molecular Sciences 20, no. 24 (December 11, 2019): 6238. http://dx.doi.org/10.3390/ijms20246238.

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A repeat expansion mutation in the C9orf72 gene is the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In this study, using multiple cell-based assay systems, we reveal both increased dipeptide repeat protein (DRP) toxicity in primary neurons and in differentiated neuronal cell lines. Using flow cytometry and confocal laser scanning microscopy of cells treated with fluorescein isothiocyanate (FITC)-labeled DRPs, we confirm that poly-glycine-arginine (GR) and poly-proline-arginine (PR) DRPs entered cells more readily than poly-glycine-proline (GP) and poly-proline-alanine (PA) DRPs. Our findings suggest that the toxicity of C9-DRPs may be influenced by properties associated with differentiated and aging motor neurons. Further, our findings provide sensitive cell-based assay systems to test phenotypic rescue ability of potential interventions.

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9

Nango, Hiroshi, Yasuhiro Kosuge, Nana Yoshimura, Hiroko Miyagishi, Takanori Kanazawa, Kaname Hashizaki, Toyofumi Suzuki, and Kumiko Ishige. "The Molecular Mechanisms Underlying Prostaglandin D2-Induced Neuritogenesis in Motor Neuron-Like NSC-34 Cells." Cells 9, no. 4 (April 10, 2020): 934. http://dx.doi.org/10.3390/cells9040934.

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Prostaglandins are a group of physiologically active lipid compounds derived from arachidonic acid. Our previous study has found that prostaglandin E2 promotes neurite outgrowth in NSC-34 cells, which are a model for motor neuron development. However, the effects of other prostaglandins on neuronal differentiation are poorly understood. The present study investigated the effect of prostaglandin D2 (PGD2) on neuritogenesis in NSC-34 cells. Exposure to PGD2 resulted in increased percentages of neurite-bearing cells and neurite length. Although D-prostanoid receptor (DP) 1 and DP2 were dominantly expressed in the cells, BW245C (a DP1 agonist) and 15(R)-15-methyl PGD2 (a DP2 agonist) had no effect on neurite outgrowth. Enzyme-linked immunosorbent assay demonstrated that PGD2 was converted to 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) under cell-free conditions. Exogenously applied 15d-PGJ2 mimicked the effect of PGD2 on neurite outgrowth. GW9662, a peroxisome proliferator-activated receptor–gamma (PPARγ) antagonist, suppressed PGD2-induced neurite outgrowth. Moreover, PGD2 and 15d-PGJ2 increased the protein expression of Islet-1 (the earliest marker of developing motor neurons), and these increases were suppressed by co-treatment with GW9662. These results suggest that PGD2 induces neuritogenesis in NSC-34 cells and that PGD2-induced neurite outgrowth was mediated by the activation of PPARγ through the metabolite 15d-PGJ2.

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10

Maier, Oliver, Julia Böhm, Michael Dahm, Stefan Brück, Cordian Beyer, and Sonja Johann. "Differentiated NSC-34 motoneuron-like cells as experimental model for cholinergic neurodegeneration." Neurochemistry International 62, no. 8 (June 2013): 1029–38. http://dx.doi.org/10.1016/j.neuint.2013.03.008.

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11

Nango, Hiroshi, Yasuhiro Kosuge, Masaki Sato, Yoshiyuki Shibukawa, Masakazu Tazaki, Yoshihisa Ito, and Kumiko Ishige. "Prostaglandin E2 induces differentiation of NSC-34 cells with neuron-like features." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO4–1–56. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po4-1-56.

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12

Martinez, Alejandra M., Jovan Mirkovic, Zofia A. Stanisz, Fahmida S. Patwari, and Wan Seok Yang. "NSC ‐34 motor neuron‐like cells are sensitized to ferroptosis upon differentiation." FEBS Open Bio 9, no. 4 (February 23, 2019): 582–93. http://dx.doi.org/10.1002/2211-5463.12577.

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13

Chen, Pei-Chun, Jing-Syuna Ruan, and Sheng-Nan Wu. "Evidence of Decreased Activity in Intermediate-Conductance Calcium-Activated Potassium Channels During Retinoic Acid–Induced Differentiation in Motor Neuron–Like NSC-34 Cells." Cellular Physiology and Biochemistry 48, no. 6 (2018): 2374–88. http://dx.doi.org/10.1159/000492653.

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Background/Aims: Intermediate-conductance Ca2+-activated K+ (IKCa; KCa3.1 or KCNN4) channels affect the behaviors of central neurons including motor neurons. The mechanism through which neuronal differentiation is related to the activity of these channels remains largely unclear. Methods: By using various molecular biology tools and electrophysiological measurements, we investigated possible changes in the activity of IKCa channels in a retinoic acid (RA)-induced differentiation process in motor neuron-like NSC-34 cells. Results: The protein and messenger RNA expression of KCa3.1 substantially diminished as NSC-34 cells were differentiated with low serum (1%) and 1 µM RA. In whole-cell current recordings, the density of delayed-rectifier K+ currents obtained from differentiated cells was elevated. However, the density of a ramp pulse-elicited K+ current that was sensitive to blockage by 1-((2-chlorophenyl) (diphenyl)methyl)-1H-pyrazole (TRAM-34)—an inhibitor of IKCa channels—was significantly higher in undifferentiated NSC-34 cells than in differentiated cells. In undifferentiated cells, the activity of IKCa channels was readily detected and the probability of channel openings was resistant to stimulation by diazoxide or suppression by verruculogen. Furthermore, this probability was increased by 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one or 9-phenanthrol and reduced by TRAM-34. The channel-opening probability decreased in RA-induced differentiated cells, whereas the single-channel conductance of IKCa channels did not differ between undifferentiated and differentiated cells. Moreover, the slow component of the mean closed time in these channels was significantly shorter in undifferentiated cells than in differentiated cells; however, the mean open time in the channel remained unchanged as cells were differentiated. Conclusion: RA-induced differentiation in neurons could exert a suppressive effect on the activity of IKCa channels.

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14

Chen, Tong, Bradley J. Turner, Philip M. Beart, Lucy Sheehan-Hennessy, Chinasom Elekwachi, and Hakan Muyderman. "Glutathione monoethyl ester prevents TDP-43 pathology in motor neuronal NSC-34 cells." Neurochemistry International 112 (January 2018): 278–87. http://dx.doi.org/10.1016/j.neuint.2017.08.009.

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15

Chiricosta, Luigi, Agnese Gugliandolo, Giuseppe Tardiolo, Placido Bramanti, and Emanuela Mazzon. "Transcriptomic Analysis of MAPK Signaling in NSC-34 Motor Neurons Treated with Vitamin E." Nutrients 11, no. 5 (May 15, 2019): 1081. http://dx.doi.org/10.3390/nu11051081.

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Vitamin E family is composed of different tocopherols and tocotrienols that are well-known as antioxidants but that exert also non-antioxidant effects. Oxidative stress may be involved in the progression of neurodegenerative disorders including amyotrophic lateral sclerosis (ALS), characterized by motor neuron death. The aim of the study was the evaluation of the changes induced in the transcriptional profile of NSC-34 motor neurons treated with α-tocopherol. In particular, cells were treated for 24 h with 10 µM α-tocopherol, RNA was extracted and transcriptomic analysis was performed using Next Generation Sequencing. Vitamin E treatment modulated MAPK signaling pathway. The evaluation revealed that 34 and 12 genes, respectively belonging to “Classical MAP kinase pathway” and “JNK and p38 MAP kinase pathway”, were involved. In particular, a downregulation of the genes encoding for p38 (Log2 fold change −0.87 and −0.67) and JNK (Log2 fold change −0.16) was found. On the contrary, the gene encoding for ERK showed a higher expression in cells treated with vitamin E (Log2 fold change 0.30). Since p38 and JNK seem more involved in cell death, while ERK in cell survival, the data suggested that vitamin E treatment may exert a protective role in NSC-34 motor neurons. Moreover, Vitamin E treatment reduced the expression of the genes which encode proteins involved in mitophagy. These results indicate that vitamin E may be an efficacious therapy in preventing motor neuron death, opening new strategies for those diseases that involve motor neurons, including ALS.

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16

Nango, Hiroshi, Yasuhiro Kosuge, Hiroko Miyagishi, Kosuke Sugawa, Yoshihisa Ito, and Kumiko Ishige. "Prostaglandin E2 facilitates neurite outgrowth in a motor neuron-like cell line, NSC-34." Journal of Pharmacological Sciences 135, no. 2 (October 2017): 64–71. http://dx.doi.org/10.1016/j.jphs.2017.09.001.

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17

Yan, Lina, Weijing Qi, Yaling Liu, Fuling Zhou, Yafei Wang, Lin Bai, Xiaomeng Zhou, et al. "The Protective Effect of Aromatase on NSC-34 Cells with Stably Expressed hSOD1-G93A." Neuroscience 411 (July 2019): 37–46. http://dx.doi.org/10.1016/j.neuroscience.2019.05.022.

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18

MEDRADO-FARIA, MARCILIA DE A., JOSÉ WILSON R. DE ALMEIDA, DIRCE M. T. ZANETTA, and GILKA J. F. GATTÁS. "Nervous system cancer mortality in an industrialized area of Brazil 1980 - 1993." Arquivos de Neuro-Psiquiatria 58, no. 2B (June 2000): 412–17. http://dx.doi.org/10.1590/s0004-282x2000000300003.

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OBJECTIVES: The industrialization process and nervous system cancer (NSC) mortality in a urban region of Brazil. METHOD: From registries of the State System of Data Analysis Foundation (SEADE), 103 males deaths by NSC (ICD-9) in Baixada Santista (BS), from 1980 to 1993 were selected. Mortality ratios were calculated comparing the standardized mortality rate for ages over 10 years old (G1) and for the age group from 35 to 64 years old, in the industrialized and non-industrialized areas in three periods: 1980-1993, 1980-86, 1987-93. RESULTS: A statiscally significant high mortality was observed in the industrialized area, for ages over 10 in all periods and only from 1980 to 1993 for ages from 34 to 64. The highest mortality ratio occurred from 1980-86 for ages over 10 - 4.12 (CI 1.79-9.42). CONCLUSION: High mortality was probably related to the environmental and occupational exposure to many organic and inorganic chemical substances, considered carcinogenics, such as aliphatic and aromatic hydrocarbons, organochlorinated, formaldehyde, nitrogenated compounds and heavy metals, found in the port and industrial complex. We discuss the importance of case-control studies in characterizing the association of these and other risk factors in the determination of NSC.

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19

Matusica, Dusan, Matthew P. Fenech, Mary-Louise Rogers, and Robert A. Rush. "Characterization and use of the NSC-34 cell line for study of neurotrophin receptor trafficking." Journal of Neuroscience Research 86, no. 3 (2008): 553–65. http://dx.doi.org/10.1002/jnr.21507.

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20

Chen, Yiquan, Bruce J. Brew, and Gilles J. Guillemin. "Characterization of the kynurenine pathway in NSC-34 cell line: implications for amyotrophic lateral sclerosis." Journal of Neurochemistry 118, no. 5 (January 28, 2011): 816–25. http://dx.doi.org/10.1111/j.1471-4159.2010.07159.x.

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21

Takano, T., M. Takigawa, E. Shirai, K. Nakagawa, M. Sakuda, and F. Suzuki. "The Effect of Parathyroid Hormone (1-34) on Cyclic AMP Level, Ornithine Decarboxylase Activity, and Glycosaminoglycan Synthesis of Chondrocytes from Mandibular Condylar Cartilage, Nasal Septal Cartilage, and Spheno-occipital Synchondrosis in Culture." Journal of Dental Research 66, no. 1 (January 1987): 84–87. http://dx.doi.org/10.1177/00220345870660011801.

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Previously, we reported methods for isolating chondrocytes from the craniofacial complex and their culture in vitro. The response of these chondrocyte cultures to bovine parathyroid hormone (1—34) (PTH) has now been investigated. PTH stimulated glycosaminoglycan (GAG) synthesis, a characteristic of the cartilage phenotype in cultured chondrocytes isolated from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS). These stimulations of GAG synthesis by PTH were dose-dependent. PTH also increased accumulation of cyclic AMP (cAMP) and the activity of ornithine decarboxylase (ODC), a rate-limiting enzyme in polyamine biosynthesis. However, PTH did not stimulate DNA synthesis. The increases in the cAMP level, ODC activity, and GAG synthesis after addition of PTH (10-7 mol/L) were greatest in MCCchondrocytes and least in NSC-chondrocytes. The difference in the responses to PTH of these three types of chondrocytes may reflect differences of the characteristics of these cells in vivo.

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22

Rajan, Thangavelu Soundara, Francesca Diomede, Placido Bramanti, Oriana Trubiani, and Emanuela Mazzon. "Conditioned medium from human gingival mesenchymal stem cells protects motor-neuron-like NSC-34 cells against scratch-injury-induced cell death." International Journal of Immunopathology and Pharmacology 30, no. 4 (November 15, 2017): 383–94. http://dx.doi.org/10.1177/0394632017740976.

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Neuronal cell death is a normal process during central nervous system (CNS) development and is also involved in the death of motor neurons in diverse spinal motor neuron degenerative diseases. Here, we investigated the neuroprotective effect of secretory factors released from human gingival mesenchymal stem cells (hGMSCs) in mechanically injured murine motor-neuron-like NSC-34 cells. The cells were exposed to scratch injury and the markers for apoptosis and oxidative stress were examined. Immunocytochemistry results showed that proapoptotic markers cleaved caspase-3 and Bax were elevated while anti-apoptotic protein Bcl-2 was suppressed in scratch-injured NSC-34 cells. Oxidative stress markers SOD-1, inducible nitric oxide synthase (iNOS), Cox-2, and proinflammatory cytokine tumor necrosis factor alpha (TNF-α) were activated. Conditioned medium (CM) derived from hGMSCs (hGMSC-CM) significantly blocked the cell death by suppressing SOD-1, iNOS, TNF-α, cleaved caspase-3, and Bax. Bcl-2 and anti-inflammatory cytokine anti-interleukin 10 (IL-10) were increased in hGMSC-CM-treated injured cells. Moreover, hGMSC-CM treatment upregulated neurotrophins anti-brain-derived neurotrophic factor (BDNF) and NT3. Western blot data of hGMSC-CM revealed the presence of neurotrophins nerve growth factor (NGF), NT3, anti-inflammatory cytokines IL-10, and transforming growth factor beta (TGF-β), suggesting their positive role to elicit neuroprotection. Our results propose that hGMSC-CM may serve as a simple and potential autologous therapeutic tool to treat motor neuron injury.

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23

WANG, FUMIN, YUCHENG LU, FAYING QI, QUANPING SU, LONG WANG, CUIPING YOU, FENGYUAN CHE, and JIXU YU. "Effect of the human SOD1-G93A gene on the Nrf2/ARE signaling pathway in NSC-34 cells." Molecular Medicine Reports 9, no. 6 (March 28, 2014): 2453–58. http://dx.doi.org/10.3892/mmr.2014.2087.

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24

Lim, Jung-Geun, Jang-Jun Lee, Sung-Hee Park, Jae-Hyung Park, Sun-Joo Kim, Ho-Chan Cho, Won-Ki Baek, Dae-Kwang Kim, and Dae-Kyu Song. "Glucagon-like peptide-1 protects NSC-34 motor neurons against glucosamine through Epac-mediated glucose uptake enhancement." Neuroscience Letters 479, no. 1 (July 2010): 13–17. http://dx.doi.org/10.1016/j.neulet.2010.05.017.

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25

Cho, Goang-Won, Ga-Young Kim, Soojeong Baek, Heejaung Kim, Taikon Kim, Hee Jin Kim, and Seung Hyun Kim. "Recombinant human erythropoietin reduces aggregation of mutant Cu/Zn-binding superoxide dismutase (SOD1) in NSC-34 cells." Neuroscience Letters 504, no. 2 (October 2011): 107–11. http://dx.doi.org/10.1016/j.neulet.2011.09.008.

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26

Babetto, Elisabetta, Alessandra Mangolini, Milena Rizzardini, Monica Lupi, Laura Conforti, Paola Rusmini, Angelo Poletti, and Lavinia Cantoni. "Tetracycline-regulated gene expression in the NSC-34-tTA cell line for investigation of motor neuron diseases." Molecular Brain Research 140, no. 1-2 (October 2005): 63–72. http://dx.doi.org/10.1016/j.molbrainres.2005.07.010.

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27

Chapman, Laurie Ann, and Hing Man Chan. "Inorganic mercury pre-exposures protect against methyl mercury toxicity in NSC-34 (neuron×spinal cord hybrid) cells." Toxicology 132, no. 2-3 (February 1999): 167–78. http://dx.doi.org/10.1016/s0300-483x(98)00151-6.

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28

Johann, S., M. Dahm, M. Kipp, U. Zahn, and C. Beyer. "Regulation of Choline Acetyltransferase Expression by 17β-Oestradiol in NSC-34 Cells and in the Spinal Cord." Journal of Neuroendocrinology 23, no. 9 (August 11, 2011): 839–48. http://dx.doi.org/10.1111/j.1365-2826.2011.02192.x.

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29

Wu, S. N., C. C. Yeh, H. C. Huang, E. C. So, and Y. C. Lo. "Electrophysiological characterization of sodium-activated potassium channels in NG108-15 and NSC-34 motor neuron-like cells." Acta Physiologica 206, no. 2 (April 25, 2012): 120–34. http://dx.doi.org/10.1111/j.1748-1716.2012.02438.x.

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30

Lee, Seok-Ho, Na-Young Choi, Hyun-Jeung Yu, Jinse Park, Hojin Choi, Kyu-Yong Lee, Yong-Min Huh, Young Joo Lee, and Seong-Ho Koh. "Atorvastatin Protects NSC-34 Motor Neurons Against Oxidative Stress by Activating PI3K, ERK and Free Radical Scavenging." Molecular Neurobiology 53, no. 1 (January 11, 2015): 695–705. http://dx.doi.org/10.1007/s12035-014-9030-0.

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31

Shantanu, Shubham, K. Vijayalakshmi, S. Shruthi, B. K. Chandrasekhar Sagar, T. N. Sathyaprabha, A. Nalini, Trichur R. Raju, and Phalguni Anand Alladi. "VEGF alleviates ALS-CSF induced cytoplasmic accumulations of TDP-43 and FUS/TLS in NSC-34 cells." Journal of Chemical Neuroanatomy 81 (April 2017): 48–52. http://dx.doi.org/10.1016/j.jchemneu.2017.01.007.

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32

Mazibuko, Zamanzima, Sunaina Indermun, Mershen Govender, Pradeep Kumar, Lisa C. Du Toit, Yahya E. Choonara, Girish Modi, Dinesh Naidoo, and Viness Pillay. "Targeted Delivery of Amantadine-loaded Methacrylate Nanosphere-ligands for the Potential Treatment of Amyotrophic Lateral Sclerosis." Journal of Pharmacy & Pharmaceutical Sciences 21 (March 30, 2018): 94–109. http://dx.doi.org/10.18433/jpps29595.

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Purpose. This study aimed to develop and analyse poly(DL-lactic acid)-methacrylic acid nanospheres bound to the chelating ligand diethylenetriaminepentaacetic acid (DTPA) for the targeted delivery of amantadine in Amyotrophic Lateral Sclerosis (ALS). Methods. The nanospheres were prepared by a double emulsion solvent evaporation technique statistically optimized employing a 3-Factor Box-Behnken experimental design. Analysis of the particle size, zeta potential, polydispersity (Pdl), morphology, drug entrapment and drug release kinetics were carried out. Results. The prepared nanospheres were determined to have particle sizes ranging from 68.31 to 113.6 nm (Pdl ≤ 0.5). An initial burst release (50% of amantadine released in 24 hr) was also obtained, followed by a prolonged release phase of amantadine over 72 hr. Successful conjugation of the chelating ligand onto the surface of the optimised nanospheres was thereafter achieved and confirmed by TEM. The synthesized modified nanospheres were spherical in shape, 105.6 nm in size, with a PdI of 0.24 and zeta potential of -28.0 mV. Conjugation efficiency was determined to be 74%. In vitro and ex vivo cell study results confirmed the intracellular uptake of the modified nanospheres by the NSC-34 cell line and the non-cytotoxicity of the synthesized nanospheres. Conclusions. Biocompatible amantadine-loaded nanospheres were successfully designed, characterized and optimized employing the randomized Box-Behnken statistical design. Delivery of amantadine over 72 hrs was achieved, with the nanospheres being of a size capable of internalization by the NSC- 34 cells. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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Shinoda, Yasuharu, Yudai Haga, Koichiro Akagawa, and Kohji Fukunaga. "Wildtype σ1 receptor and the receptor agonist improve ALS-associated mutation-induced insolubility and toxicity." Journal of Biological Chemistry 295, no. 51 (October 14, 2020): 17573–87. http://dx.doi.org/10.1074/jbc.ra120.015012.

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Genetic mutations related to ALS, a progressive neurological disease, have been discovered in the gene encoding σ-1 receptor (σ1R). We previously reported that σ1RE102Q elicits toxicity in cells. The σ1R forms oligomeric states that are regulated by ligands. Nevertheless, little is known about the effect of ALS-related mutations on oligomer formation. Here, we transfected NSC-34 cells, a motor neuronal cell line, and HEK293T cells with σ1R-mCherry (mCh), σ1RE102Q-mCh, or nontagged forms to investigate detergent solubility and subcellular distribution using immunocytochemistry and fluorescence recovery after photobleaching. The oligomeric state was determined using crosslinking procedure. σ1Rs were soluble to detergents, whereas the mutants accumulated in the insoluble fraction. Within the soluble fraction, peak distribution of mutants appeared in higher sucrose density fractions. Mutants formed intracellular aggregates that were co-stained with p62, ubiquitin, and phosphorylated pancreatic eukaryotic translation initiation factor-2-α kinase in NSC-34 cells but not in HEK293T cells. The aggregates had significantly lower recovery in fluorescence recovery after photobleaching. Acute treatment with σ1R agonist SA4503 failed to improve recovery, whereas prolonged treatment for 48 h significantly decreased σ1RE102Q-mCh insolubility and inhibited apoptosis. Whereas σ1R-mCh formed monomers and dimers, σ1RE102Q-mCh also formed trimers and tetramers. SA4503 reduced accumulation of the four types in the insoluble fraction and increased monomers in the soluble fraction. The σ1RE102Q insolubility was diminished by σ1R-mCh co-expression. These results suggest that the agonist and WT σ1R modify the detergent insolubility, toxicity, and oligomeric state of σ1RE102Q, which may lead to promising new treatments for σ1R-related ALS.

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Lai, Tzeng, Huang, and Wu. "The Novel Direct Modulatory Effects of Perampanel, an Antagonist of AMPA Receptors, on Voltage-Gated Sodium and M-type Potassium Currents." Biomolecules 9, no. 10 (October 22, 2019): 638. http://dx.doi.org/10.3390/biom9100638.

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Perampanel (PER) is a selective blocker of AMPA receptors showing efficacy in treating various epileptic disorders including brain tumor-related epilepsy and also potential in treating motor neuron disease. However, besides its inhibition of AMPA-induced currents, whether PER has any other direct ionic effects in different types of neurons remains largely unknown. We investigated the effects of PER and related compounds on ionic currents in different types of cells, including hippocampal mHippoE-14 neurons, motor neuron-like NSC-34 cells and U87 glioma cells. We found that PER differentially and effectively suppressed the amplitude of voltage-gated Na+ currents (INa) in mHippoE-14 cells. The IC50 values required to inhibit peak and late INa were 4.12 and 0.78 μM, respectively. PER attenuated tefluthrin-induced increases in both amplitude and deactivating time constant of INa. Importantly, PER also inhibited the amplitude of M-type K+ currents (IK(M)) with an IC50 value of 0.92 μM. The suppression of IK(M) was attenuated by the addition of flupirtine or ZnCl2 but not by L-quisqualic acid or sorafenib. Meanwhile, in cell-attached configuration, PER (3 μM) decreased the activity of M-type K+ channels with no change in single-channel conductance but shifting the activation curve along the voltage axis in a rightward direction. Supportively, PER suppressed IK(M) in NSC-34 cells and INa in U87 glioma cells. The inhibitory effects of PER on both INa and IK(M), independent of its antagonistic effect on AMPA receptors, may be responsible for its wide-spectrum of effects observed in neurological clinical practice.

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Lee, S. H., H. Choi, S. H. Koh, C. Shim, H. T. Kim, and J. Kim. "Atorvastatin protects NSC-34 motor neurons against oxidative stress through the activation of PI3K, ERK and free radical scavenging." Journal of the Neurological Sciences 333 (October 2013): e408. http://dx.doi.org/10.1016/j.jns.2013.07.1474.

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KEILHOFF, GERBURG, BENJAMIN LUCAS, KATJA UHDE, and HISHAM FANSA. "Selected gene profiles of stressed NSC-34 cells and rat spinal cord following peripheral nerve reconstruction and minocycline treatment." Experimental and Therapeutic Medicine 11, no. 5 (March 2, 2016): 1685–99. http://dx.doi.org/10.3892/etm.2016.3130.

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Miyagishi, Hiroko, Yasuhiro Kosuge, Yuki Yoneoka, Maiko Ozone, Manami Endo, Nobuhiro Osada, Kumiko Ishige, Kuniko Kusama-Eguchi, and Yoshihisa Ito. "Prostaglandin E2-Induced Cell Death is Mediated by Activation of EP2 Receptors in Motor Neuron-like NSC-34 Cells." Journal of Pharmacological Sciences 121, no. 4 (2013): 347–50. http://dx.doi.org/10.1254/jphs.12274sc.

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Almokhtar, Mokhtar, Kjell Wikvall, S. J. Kumari A. Ubhayasekera, Jonas Bergquist, and Maria Norlin. "Motor neuron-like NSC-34 cells as a new model for the study of vitamin D metabolism in the brain." Journal of Steroid Biochemistry and Molecular Biology 158 (April 2016): 178–88. http://dx.doi.org/10.1016/j.jsbmb.2015.12.010.

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Vijayalakshmi, K., Piyush Ostwal, R. Sumitha, S. Shruthi, Anu Mary Varghese, Poojashree Mishra, S. Gowri Manohari, et al. "Role of VEGF and VEGFR2 Receptor in Reversal of ALS-CSF Induced Degeneration of NSC-34 Motor Neuron Cell Line." Molecular Neurobiology 51, no. 3 (June 1, 2014): 995–1007. http://dx.doi.org/10.1007/s12035-014-8757-y.

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So, Edmund Cheung, King Chuen Wu, Feng Chen Kao, and Sheng Nan Wu. "Effects of midazolam on ion currents and membrane potential in differentiated motor neuron-like NSC-34 and NG108-15 cells." European Journal of Pharmacology 724 (February 2014): 152–60. http://dx.doi.org/10.1016/j.ejphar.2013.12.034.

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Gugliandolo, Agnese, Serena Silvestro, Luigi Chiricosta, Federica Pollastro, Placido Bramanti, and Emanuela Mazzon. "The Transcriptomic Analysis of NSC-34 Motor Neuron-Like Cells Reveals That Cannabigerol Influences Synaptic Pathways: A Comparative Study with Cannabidiol." Life 10, no. 10 (October 1, 2020): 227. http://dx.doi.org/10.3390/life10100227.

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More than 120 cannabinoids were isolated from Cannabis sativa. In particular, Cannabidiol (CBD) and Cannabigerol (CBG) represent the two most studied non-psychoactive cannabinoids. However, CBG is less studied and less data are available on its biological properties and influence on synaptic transmission. On the contrary, CBD is already known to modulate brain excitatory glutamate, inhibitory γ-aminobutyric acid (GABA) and dopamine neurotransmission. In this study, using Next-Generation Sequencing (NGS) technology, we evaluated how CBG (1 or 5 µM) and CBD (1 or 5 µM) influence the transcriptome of the main neurotransmission pathways in NSC-34 motor neuron-like cells. At first, we evaluated that CBG and CBD were not cytotoxic and decreased the expression of pro-apoptotic genes. CBG and CBD are able to influence the expression of the genes involved in glutamate, GABA and dopamine signaling. Interestingly, the transcriptional changes induced by CBG were similar compared to CBD.

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Daniel, Bareket, Omer Green, Olga Viskind, and Arie Gruzman. "Riluzole increases the rate of glucose transport in L6 myotubes and NSC-34 motor neuron-like cells via AMPK pathway activation." Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 14, no. 5-6 (July 8, 2013): 434–43. http://dx.doi.org/10.3109/21678421.2013.808226.

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Benavente, Francisca, Cristina Pinto, Margarita Parada, Juan Pablo Henríquez, and Nelson Osses. "Bone morphogenetic protein 2 inhibits neurite outgrowth of motor neuron-like NSC-34 cells and up-regulates its type II receptor." Journal of Neurochemistry 122, no. 3 (June 12, 2012): 594–604. http://dx.doi.org/10.1111/j.1471-4159.2012.07795.x.

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Nango, Hiroshi, Yasuhiro Kosuge, Yuri Aono, Tadashi Saigusa, Yoshihisa Ito, and Kumiko Ishige. "Characterization of inductions of neurite outgrowth and neuronal markers in NSC-34 cells during differentiation with prostaglandin E₂." Proceedings for Annual Meeting of The Japanese Pharmacological Society 92 (2019): 2—P—098. http://dx.doi.org/10.1254/jpssuppl.92.0_2-p-098.

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Herrando-Grabulosa, Mireia, Caty Casas, Kevin Talbot, and José Aguilera. "Neurotrophic Properties of C-Terminal Domain of the Heavy Chain of Tetanus Toxin on Motor Neuron Disease." Toxins 12, no. 10 (October 21, 2020): 666. http://dx.doi.org/10.3390/toxins12100666.

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The carboxyl-terminal domain of the heavy chain of tetanus toxin (Hc-TeTx) exerts a neuroprotective effect in neurodegenerative diseases via the activation of signaling pathways related to neurotrophins, and also through inhibiting apoptotic cell death. Here, we demonstrate that Hc-TeTx preserves motoneurons from chronic excitotoxicity in an in vitro model of amyotrophic lateral sclerosis. Furthermore, we found that PI3-K/Akt pathway, but not p21ras/MAPK pathway, is involved in their beneficial effects under chronic excitotoxicity. Moreover, we corroborate the capacity of the Hc-TeTx to be transported retrogradely into the spinal motor neurons and also its capacity to bind to the motoneuron-like cell line NSC-34. These findings suggest a possible therapeutic tool to improve motoneuron preservation in neurodegenerative diseases such as amyotrophic lateral sclerosis.

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Desai, Virendra Rajendrakumar, Saeed Sam Sadrameli, Amanda V. Jenson, Samuel K. Asante, Bradley Daniels, Todd W. Trask, and Gavin Britz. "Ventriculoperitoneal shunt complications in an adult population: A comparison of various shunt designs to prevent overdrainage." Surgical Neurology International 11 (September 5, 2020): 269. http://dx.doi.org/10.25259/sni_38_2020.

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Background: Overdrainage after cerebrospinal fluid diversion remains a significant morbidity. The hydrostatic, gravitational force in the upright position can aggravate this. Siphon control (SC) mechanisms, as well as programmable and flow regulating devices, were developed to counteract this. However, limited studies have evaluated their safety and efficacy. In this study, direct comparisons of the complication rates between siphon control (SC) and non-SC (NSC), fixed versus programmable, and flow- versus pressure regulating valves are undertaken. Methods: A retrospective chart review was performed over all shunt implantations from January 2011 to December 2016 within the Houston Methodist Hospital system. Complication rates within 6 months of the operative date, including infection, subdural hematoma, malfunction, and any other shunt-related complication, were analyzed via Fisher’s exact test, with P < 0.05 regarded as significant. Subgroup analyses based on diagnoses – normal pressure hydrocephalus (HCP), pseudotumor cerebri, or other HCP – were also performed. Results: The overall shunt-related complication rate in this study was 19%. Overall rates of infection, shunt failure, and readmission within 180 days were 3%, 11%, and 34%, respectively. No difference was seen between SC and NSC groups in any complication rate overall or on subgroup analyses. When comparing fixed versus programmable and flow- versus pressure-regulating valves, the latter in each analysis had significantly lower malfunction and total complication rates. Conclusions: Programmable and pressure regulating devices may lead to lower shunt malfunction and total complication rates. Proper patient selection should guide valve choice. Future prospective studies may further elucidate the difference in complication rates between these various shunt designs.

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Raghavan, D., P. Gianoutsos, J. Bishop, J. Lee, I. Young, P. Corte, P. Bye, and B. McCaughan. "Phase II trial of carboplatin in the management of malignant mesothelioma." Journal of Clinical Oncology 8, no. 1 (January 1990): 151–54. http://dx.doi.org/10.1200/jco.1990.8.1.151.

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Thirty-one patients with advanced malignant mesothelioma, previously untreated or having received only one prior cytotoxic regimen, were treated in a prospective, single-arm phase II trial with carboplatin (NSC 241240) at a dose of 150 mg/m2 per day intravenously (IV) for 3 days (450 mg/m2/course). One complete remission and four partial remissions were achieved, yielding an overall objective response rate of 16% (95% confidence interval [CI], 5.4% to 34%). The median duration of remission was 8 months (range, 5 to 17). Nonhematological toxicity was mild (only 12% with World Health Organization [WHO] grade 3 vomiting); 16% suffered WHO grade 3 to 4 hematological toxicity, but there were no life-threatening episodes and no treatment-related deaths. Carboplatin has modest activity against malignant mesothelioma and, because of its low toxicity, has a role in the management of this disease.

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Jiang, Xian-Peng, Catherine C. Baucom, and Robert L. Elliott. "Mitochondria Dynamically Transplant into Cells in Vitro and in Mice and Rescue Aerobic Respiration of Mitochondrial DNA-Depleted Motor Neuron NSC-34." Journal of Biomedical Science and Engineering 13, no. 09 (2020): 203–21. http://dx.doi.org/10.4236/jbise.2020.139019.

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Madison, Roger D., Christopher McGee, Renee Rawson, and Grant A. Robinson. "Extracellular vesicles from a muscle cell line (C2C12) enhance cell survival and neurite outgrowth of a motor neuron cell line (NSC-34)." Journal of Extracellular Vesicles 3, no. 1 (January 2014): 22865. http://dx.doi.org/10.3402/jev.v3.22865.

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Moreno-Martet, Miguel, Leyre Mestre, Frida Loría, Carmen Guaza, Javier Fernández-Ruiz, and Eva de Lago. "Identification of receptors and enzymes for endocannabinoids in NSC-34 cells: Relevance for in vitro studies with cannabinoids in motor neuron diseases." Neuroscience Letters 508, no. 2 (February 2012): 67–72. http://dx.doi.org/10.1016/j.neulet.2011.12.020.

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