Littérature scientifique sur le sujet « 158N oligodendroglial cell line »
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Articles de revues sur le sujet "158N oligodendroglial cell line"
ROSE, LYNN M., SUSANNE L. JACKEVICIUS et EDWARD A. CLARK. « Expression of Leukocyte Antigens on an Oligodendroglial Cell Line ». Annals of the New York Academy of Sciences 540, no 1 Advances in N (novembre 1988) : 455–58. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27132.x.
Texte intégralSchuster, Norbert, Herdis Bender, Anja Philippi, Srinivasa Subramaniam, Jens Strelau, Ziyuan Wang et Kerstin Krieglstein. « TGF- ? induces cell death in the oligodendroglial cell line OLI-neu ». Glia 40, no 1 (16 septembre 2002) : 95–108. http://dx.doi.org/10.1002/glia.10110.
Texte intégralJin, Ying, Melanie L. McEwen, M. Said Ghandour et Joe E. Springer. « Overexpression of XIAP Inhibits Apoptotic Cell Death in an Oligodendroglial Cell Line ». Cellular and Molecular Neurobiology 24, no 6 (décembre 2004) : 853–63. http://dx.doi.org/10.1007/s10571-004-6924-9.
Texte intégralFukatsu, Shoya, Yuki Miyamoto, Yu Oka, Maki Ishibashi, Remina Shirai, Yuki Ishida, Shin Endo, Hironori Katoh et Junji Yamauchi. « Investigating the Protective Effects of a Citrus Flavonoid on the Retardation Morphogenesis of the Oligodendroglia-like Cell Line by Rnd2 Knockdown ». Neurology International 16, no 1 (26 décembre 2023) : 33–61. http://dx.doi.org/10.3390/neurolint16010003.
Texte intégralSawaguchi, Sui, Rimi Suzuki, Hiroaki Oizumi, Katsuya Ohbuchi, Kazushige Mizoguchi, Masahiro Yamamoto, Yuki Miyamoto et Junji Yamauchi. « Hypomyelinating Leukodystrophy 8 (HLD8)-Associated Mutation of POLR3B Leads to Defective Oligodendroglial Morphological Differentiation Whose Effect Is Reversed by Ibuprofen ». Neurology International 14, no 1 (16 février 2022) : 212–44. http://dx.doi.org/10.3390/neurolint14010018.
Texte intégralIssa, Y., D. C. Watts, A. J. Duxbury, P. A. Brunton, M. B. Watson et C. M. Waters. « Mercuric chloride : toxicity and apoptosis in a human oligodendroglial cell line MO3.13 ». Biomaterials 24, no 6 (mars 2003) : 981–87. http://dx.doi.org/10.1016/s0142-9612(02)00436-2.
Texte intégralNaffaa, Vanessa, Isabelle Hochar, Chéryane Lama, Romain Magny, Anne Regazzetti, Pierre Gressens, Olivier Laprévote, Nicolas Auzeil et Anne-Laure Schang. « Bisphenol A Impairs Lipid Remodeling Accompanying Cell Differentiation in the Oligodendroglial Cell Line Oli-Neu ». Molecules 27, no 7 (31 mars 2022) : 2274. http://dx.doi.org/10.3390/molecules27072274.
Texte intégralTorii, Tomohiro, Remina Shirai, Risa Kiminami, Satoshi Nishino, Takanari Sato, Sui Sawaguchi, Nana Fukushima, Yoichi Seki, Yuki Miyamoto et Junji Yamauchi. « Hypomyelinating Leukodystrophy 10 (HLD10)-Associated Mutations of PYCR2 Form Large Size Mitochondria, Inhibiting Oligodendroglial Cell Morphological Differentiation ». Neurology International 14, no 4 (16 décembre 2022) : 1062–80. http://dx.doi.org/10.3390/neurolint14040085.
Texte intégralBello-Morales, Raquel, Marta Pérez-Hernández, María Teresa Rejas, Fuencisla Matesanz, Antonio Alcina et José Antonio López-Guerrero. « Interaction of PLP with GFP-MAL2 in the Human Oligodendroglial Cell Line HOG ». PLoS ONE 6, no 5 (9 mai 2011) : e19388. http://dx.doi.org/10.1371/journal.pone.0019388.
Texte intégralCraighead, Mark, Jessica Pole et Catherine Waters. « Caspases mediate C2-ceramide-induced apoptosis of the human oligodendroglial cell line, MO3.13 ». Neuroscience Letters 278, no 3 (janvier 2000) : 125–28. http://dx.doi.org/10.1016/s0304-3940(99)00866-6.
Texte intégralThèses sur le sujet "158N oligodendroglial cell line"
Padilla, Ferrer Aïda. « ADAM10 in myelination of the central nervous system : study of ADAM10 localization and development of an inducible oligodendroglial ADAM10 knock out (KOOLA10) mouse strain ». Electronic Thesis or Diss., Université Paris Cité, 2022. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=4270&f=41801.
Texte intégralIn the central nervous system (CNS), oligodendrocytes (OL) envelop the axons with their membrane extensions, forming the myelin sheath. The OL death and the loss of myelin (demyelination) occur in demyelinating diseases such as multiple sclerosis, for which there is no specific cure nowadays. Our goal is to enhance an endogenous repair process via the ADAM10/sAPPa pathway. The Amyloid Precursor Protein (APP) can be cleaved by a-secretases, members of the ADAM (A Desintegrin And Metalloprotease) family such as ADAM10, the main a-secretase in the CNS. The enzymatic cleavage of APP generates a neuroprotective soluble peptide called sAPPa. Our previous results showed that the pharmacological activation of a-secretases was able to enhance OL differentiation in vitro, to promote myelin protection from demyelination, to enhance remyelination ex vivo and in vivo and to improve the locomotor function. The aim of my thesis was, thus, to further investigate the role of oligodendroglial ADAM10 in myelin formation and maintenance. Three lines of investigation have been pursued. The first aim was to investigate the regional and cellular expression of ADAM10 in the CNS by immunolabeling of ADAM10 protein in adult mice and in primary neuronal and glial cultures. ADAM10 was widely expressed in brain, cerebellum and spinal cord with high expression in the hippocampus and piriform cortex. Neurons expressed much more ADAM10 than glial cells in CNS tissues and in vitro we were able to detect ADAM10 in neurons, OL, astrocytes and microglia. The second aim was to investigate the role of oligodendroglial ADAM10 in myelination. Therefore, we have created a novel mouse strain (KOOLA10) that allows the deletion of OL ADAM10 at specific time points related to the process of oligodendrogenesis and myelination. In this mouse strain, the deficiency is induced by the excision of the exon 3 of Adam10 gene flanked by 2 loxP sequences by the Cre recombinase, which is under the control of the PLP (Proteolipid Protein) promoter. When ADAM10 deficiency was induced at birth during oligodendrogenesis, an impairment in exploratory activity was observed at P21 but it was compensated later on. When ADAM10 deficiency was induced during myelin maintenance in adult mice, the aforementioned behavior worsened over time. Further analysis is still required to explain the behavioral changes observed in KO mice. Surprisingly, the level of MBP (Myelin Basic Protein), assessed by western blot and immunohistological studies, did not show an apparent change in KO mice. The third aim was to investigate the role of ADAM10 in OL development and functionality. The ADAM10 knock-down using siRNA in the 158N OL cell line did not modify cell morphology, proliferation or migration but it induced a decrease in myelin gene expression. To validate these results, we set up a new OL primary cell isolation and culture protocol. Preliminary results also pointed to a reduction of myelin genes expression in ADAM10-deficient OL. Finally, we used organotypic culture of cerebellum, highly rich in myelin, to address the effect of ADAM10 deficiency. We set up a transfection protocol to knock down ADAM10 in cerebellar slices and further focused on the study of myelination in KOOLA10. A significant decrease in the number of myelinated axons was observed in cerebellar slices from KO mice after demyelination, suggesting a beneficial effect of OL ADAM10 in myelin protection or repair. In conclusion, I have shown the distribution of ADAM10 in the CNS, generated the KOOLA10 mouse strain and set up different protocols and tools that allow the investigation of the role of oligodendroglial ADAM10 in myelination. I have obtained evidence suggesting that OL ADAM10 affects exploratory behavior and myelin and is necessary for myelin protection and/or repair. Further investigation is required to better decipher the role of OL ADAM10 in myelin maintenance, and CNS re/myelination