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Academic literature on the topic 'NSC-34'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "NSC-34"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "NSC-34"

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Matusica, Dusan, and matu0012@flinders edu au. "Regulation of p75NTR Trafficking by Neurotrophins in the NSC-34 Motor Neuron Cell Line." Flinders University. School Of Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20080808.115027.

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Neurotrophins are a family of growth factors necessary for the development and maintenance of the nervous system. They produce their effects through receptor mediated signaling mechanisms that are highly regulated by sophisticated intracellular transport networks. The impairment of intracellular trafficking of neurotrophins in motor neurons has been identified as one possible factor in the development of motor neuron diseases, but remains inadequately studied. Aided by advances in imaging technology and the development of more powerful and sensitive detection tools for in-vitro studies, the dynamics of intracellular transport of neurotrophins are beginning to be unraveled. However, a primary limiting factor in the study of neurotrophin-transport dynamics in motor neurons has been the lack of alternative and easily available in-vitro systems able to substitute the often difficult and costly primary motor neuron cultures. The aim of this project was to develop a suitable motor neuron model using the NSC-34 cell line for the study of receptor mediated trafficking events through endosomal transport pathways. Successful evaluation and characterization of NSC-34 cells for motor neuron specific markers would result in the investigation of the p75 neurotrophin receptor (p75NTR) trafficking pathways in the presence of exogenous neurotrophins, with a variety of confocal imaging techniques. Chapter 3 describes the optimisation of NSC-34 cell culture conditions through media modification and the development of a suitable growth substrate matrix, which significantly improved cell adhesion, differentiation and the ability to culture the cells for extended time periods in serum free conditions. Quantitative measurements of cell proliferation, culture viability, cell-body size and neurite length are described to highlight the increased value of the cell line for long-term culture and experiments examining a broad range of issues relevant to motor neurons. In Chapter 4, multiple experimental approaches were used to extensively screen the NSC-34 cell line for the presence of motor neuron-specific markers, neurotrophin receptors and proteins involved in regulation of endosomal transport. This characterization established the presence of a developing motor neuron-like neurotrophin receptor profile (p75NTR, TrkB and TrkC), a genetic marker of developing motor neurons, cholinergic markers, proteins regulating transport within the endosomal pathway, and additional proteins previously shown to directly interact with neurotrophin receptors, including sortilin, and the lipid raft associated ganglioside GT1b. Furthermore, evidence is provided that NSC-34 cells undergo apoptosis in response to exogenous nerve growth factor (NGF) or neurotrophin-3 (NT-3), but not brain derived neurotrophic factor (BDNF) or neurotrophin-4 (NT-4). In addition characterization of mouse specific p75NTR antibodies is presented to establish their suitability for internalization studies without altering the binding of exogenous neurotrophins to the receptor. Subsequent confocal microscopy examination focusing on p75NTR trafficking in Chapter 5 revealed that internalization and intracellular transport of this receptor is regulated by exogenous neurotrophins at the cell surface where ligand binding and internalization occur, and in endosomal compartments where the bulk of receptors and ligands are targeted to their specific destinations. Evidence is provided showing that p75NTR internalization is altered in the presence of NGF, NT-3, or NT-4, but not BDNF, and the receptor is diverted into non-clathrin mediated endosomal pathways in response to NGF but not BDNF. Immunofluorescence confocal microscopy suggests that p75NTR recycles to the plasma membrane in a Rab4 GTPase dependent manner in the absence of neurotrophins. Addition of neurotrophins diverted p75NTR from the recycling Rab4 positive pathway, into EEA-1 positive sorting endosomes in the presence of NGF or NT-3, or lysosomal degradation in the presence of BDNF or NT-4. This study clearly demonstrates the suitability of the NSC-34 cell line as an alternate in-vitro system for the study of motor neuron biology, particularly the study of neurotrophin receptor trafficking. Taken together the results represented in this study suggest for the first time, that the fate of the p75NTR receptor depends on which neurotrophin is bound. These findings have important implications for understanding the dynamic mechanisms of action of p75NTR in normal neuronal function, and may also offer further insight into the potential role of neurotrophins in the treatment of neurodegenerative diseases.
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Hallgren, Henrik. "Characterization of NeuN expression in the mouse neuronal NSC-34 cell line using RT-qPCR, immunological staining and siRNA-mediated gene suppression." Thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-389757.

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Background: Acute spinal trauma is followed by a secondary injury that causes additional damage to the tissue. The mouse neuronal hybrid cell line NSC-34 is planned for studies regarding this process, wherefore the cell line needed to be established in the laboratory and a proof-of-concept study needed to be performed. A suitable target gene for this study was Neuronal Nucleus (NeuN), a neuronal marker expressed in nearly all neuronal cells although not yet studied in NSC-34. Aim: The aim of this project was to characterize the expression of NeuN in differentiated and undifferentiated NSC-34 cells and silence gene expression by using siRNA. Methods: RT-qPCR was used to measure NeuN expression during passages 5 to 15 and a comparison was performed between one early and one late passage. Lipofectamine® RNAiMAX was used for siRNA-treatment in different concentrations and several different medium compositions were tested as differentiation media. Results: NeuN was expressed in passages 5 to 15, with decreased expression levels in passage 13 (ΔCt 15.36 ± 0.16) compared to passage 5 (ΔCt 15.09 ± 0.16), p < 0.05. The expression levels did not change after differentiation. siRNA-treatment yielded knockdown when using  high concentrations of the reagent (p < 0.05). Conclusion: NeuN was expressed in a stable, low level throughout passages 5 to 15 with a slightly decreased expression during later passages and no change after differentiation. The siRNA-treatment suppressed gene expression, although further optimization is needed to increase the suppression.
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Chapman, Laurie A. "Interactions of nutrients on methyl mercury toxicity in neuron X spinal chord hybrid cells (NSC-34) and human oligodendrocyte X rhabdomyosarcoma cells (MO3.13)." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36888.

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Exposure to methyl mercury (MeHg) is a global concern. Increased chronic exposure to MeHg among fish and marine mammal consuming populations will increase the risk of prenatal exposure and as a result, the risk of infant brain damage and neurotoxcity. It is therefore important to understand the role of environmental factors, such as nutrition, in determining susceptibility to MeHg toxicity. Three nutrients (selenium (Se), vitamin C and vitamin E) were selected for examination of their interactions with the mechanisms of McHg cytotoxicity in vitro. Two hybrid neural cell lines (M03.13 and NSC-34) were evaluated for their usefulness in the study of MeHg cytotoxicity. Sixteen toxic endpoints were selected for investigation of growth, viability, structure and biochemistry. Both cell lines responded to MeHg exposure in a dose dependent manner for the majority of endpoints suggesting that both MO3.13 and NSC-34 cells undergo structural and biochemical changes during exposure to McHg, but that MO3.13 cells are more sensitive to DNA, mitochondria) membrane damage and glutathione (GSH) depletion and that NSC-34 cells are more sensitive to protein damage and apoptosis. Se exposure lessened the MeHg-induced decrease in DNA and GSH concentrations in both cell lines. In NSC-34 cells, Se also increased F-actin concentrations and prevented an increase in caspase-3 activity. Se may alter the mechanism of cell death by preventing McHg disruption of DNA replication thus maintaining the production and function of peptides (GSH) and protein (polymerized actin) that aid in MeHg detoxification and neural function. In NSC-34 cells, vitamin C prevented the induction of caspase-3 activity and lessened DNA damage and GSH depletion. Vitamin E lessened GSH depletion and lessened G-actin depletion. Both vitamin C and E improved GSH status, but vitamin C also delayed McHg damage of DNA and prevented early signs of apoptosis suggesting these two vitamins interfere with MeHg metabolism by diffe
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Metternich, Rouven Marian [Verfasser]. "The SWH signalling as a key regulator for the maintenance of NSC quiescence in Drosophila melanogaster / Rouven Marian Metternich." Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/1138593699/34.

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Lin, Yu-Ting, and 林于婷. "Protective effects of naloxone on H2O2-induced cytotoxicity in mouse motor neuronal NSC-34 cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/95485642620048988069.

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碩士
高雄醫學大學
藥理學研究所
98
Increasing evidence indicates that motor neuron diseases characterized by loss of motor endplate, axonal degeneration, and cell death of motor neurons are caused by oxidative stress, mitochondrial dysfunction, protein aggregation, axonal transport defects, and inflammation. Naloxone has been reported to possess anti-inflammatory and neuroprotective effects, at least in part, by its inhibition on NADPH oxidase. The aim of this study is to investigate the protective effect of naloxone on H2O2-induced cytotoxicity in a motor neuronal cell line, NSC-34. Results indicated H2O2 decreased cell viability, down-regulated protein of survival motor neuron gene (Smn) expression, decreased mitochondria membrane potential and increased oxidative stress factors (NOX2 and intracellular reactive oxygen species, intracellular ROS). In addition, H2O2 also increased oxygen consumption rate in NSC-34. However, naloxone pre-treatment increased cell viability and Smn protein expression and attenuated oxidative stress factors, oxygen consumption and release of cytochrome c from mitochodria in H2O2-treated cells. Moreover, naloxone also attenuated H2O2-induced overexpression of cleaved-caspase-3. Naloxone increased Bcl-2/Bax ratio in H2O2-treated cells as well. Taken together, naloxone not only attenuated oxidative stress, but also up-regulated Smn protein, and modulated apoptotic and anti-apoptotic protein expression. The characterization in neuroprotective effect has potential benefits on motor neuronal degenerative diseases.
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Chiou, Hung-Shiang, and 邱鴻祥. "Stimulation of Purinergic Signaling Pathway Induces SMN Protein Expression and Neuronal Differentiation in Motor-Neuron-Like NSC-34 Cells." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/mtaqpv.

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碩士
高雄醫學大學
醫學系生理學科碩士班
103
Abstract Spinal muscular atrophy (SMA) is a genetic neurodegenerative disease. survival of motor neuron (SMN) protein has been found in cell nucleus as well as the neurite and growth cone of developing motor neurons. Nonetheless, it is still not clarified that why SMN deficiency causes neurodegeneration. In addition, accumulating evidence have shown that extracellular purines such as adenosine triphosphate (ATP) and adenosine diphosphate (ADP) act as neurotransmitters to modulate nerve synapse. Purines binds to the purinergic receptor (P2 receptor) such as P2Y1 and P2Y2 on the cell membrane of neurons, leading to an increase in intracellular calcium concentration ([Ca2+]i) and downstream signal transduction. It is proposed that in SMA, purinergic signaling pathway is compromised, leading to disruption in neuronal differentiation. We hypothesize that the disruption of SMN in motor neurons may cause disruption in purinergic signaling, contributing to neurodegeneration.We used NSC-34 cell line, a hybrid cell produced by the fusion of neuroblastoma and motor neuron, as the cell model. The neuronal differentiation of NSC-34 cells was stimulated by fetal bovine serum (FBS) and horse serum (HS). Inducible RNAi-stable NSC-34 cells were treated with doxycycline for 5 days to knock down SMN gene. The vector without an insert was also stably transfected into NSC-34 cells. Normal NSC34 cells only treated with doxycycline were used as control group. Intracellular Ca2+ homeostasis was recorded by Ca2+ imaging. Western blotting and immunofluorescence cytochemistry was used to examine SMN, neuronal marker protein α-tubulin, MAP2, synaptophysin, P2Y1 and P2Y2 receptors, total and phosphorylated IP3 receptor. We found that in SMN gene knocked down cells the neuronal differentiation was diminished and P2Y receptor-mediated calcium signaling was imparied. After knockdown of SMN, the protein expression of P2Y1 and P2Y2 purinergic receptor isoforms were decreased, and phosphorylated (i.e. inactive) IP3 receptor was increased, probably causing a disruption in purinergic signaling. In addition, stimulation by extracellular ATP increased the protein expression of SMN, while P2Y receptor antagonist RB2 blocked the stimulatory effect of ATP, and decreased the protein expression of SMN, MAP2 and synaptophysin. Our findings show that SMN protein is associated with purinergic signaling pathway and calcium homeostasis. Extracellular ATP enhanced SMN protein expression and motor neuron development. Interactions between SMN protein and purinergic signaling may play important roles in the pathogenesis of SMA.
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Conference papers on the topic "NSC-34"

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Seedat, F., J. Geppert, C. Stinton, J. Patterson, CS Brown, B. Tan, K. Freeman, et al. "OP34 Universal antenatal culture-based screening for maternal group b streptococcus (gbs) carriage to prevent early-onset gbs disease: a systematic review for the uk national screening committee (nsc)." In Society for Social Medicine, 61st Annual Scientific Meeting, University of Manchester, 5–8 September 2017. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/jech-2017-ssmabstracts.34.

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