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Published: 25 May 2024

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1

ROSE, LYNN M., SUSANNE L. JACKEVICIUS, and 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 (November 1988): 455–58. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27132.x.

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2

Schuster, Norbert, Herdis Bender, Anja Philippi, Srinivasa Subramaniam, Jens Strelau, Ziyuan Wang, and Kerstin Krieglstein. "TGF-? induces cell death in the oligodendroglial cell line OLI-neu." Glia 40, no. 1 (September 16, 2002): 95–108. http://dx.doi.org/10.1002/glia.10110.

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3

Jin, Ying, Melanie L. McEwen, M. Said Ghandour, and Joe E. Springer. "Overexpression of XIAP Inhibits Apoptotic Cell Death in an Oligodendroglial Cell Line." Cellular and Molecular Neurobiology 24, no. 6 (December 2004): 853–63. http://dx.doi.org/10.1007/s10571-004-6924-9.

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4

Fukatsu, Shoya, Yuki Miyamoto, Yu Oka, Maki Ishibashi, Remina Shirai, Yuki Ishida, Shin Endo, Hironori Katoh, and 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 (December 26, 2023): 33–61. http://dx.doi.org/10.3390/neurolint16010003.

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Recent discoveries suggest links between abnormalities in cell morphogenesis in the brain and the functional deficiency of molecules controlling signal transduction in glial cells such as oligodendroglia. Rnd2 is one such molecule and one of the Rho family monomeric GTP-binding proteins. Despite the currently known functions of Rnd2, its precise roles as it relates to cell morphogenesis and disease state remain to be elucidated. First, we showed that signaling through the loss of function of the rnd2 gene affected the regulation of oligodendroglial cell-like morphological differentiation using the FBD-102b cell line, which is often utilized as a differentiation model. The knockdown of Rnd2 using the clustered regularly interspaced palindromic repeats (CRISPR)/CasRx system or RNA interference was shown to slow morphological differentiation. Second, the knockdown of Prag1 or Fyn kinase, a signaling molecule acting downstream of Rnd2, slowed differentiation. Rnd2 or Prag1 knockdown also decreased Fyn phosphorylation, which is critical for its activation and for oligodendroglial cell differentiation and myelination. Of note, hesperetin, a citrus flavonoid with protective effects on oligodendroglial cells and neurons, can recover differentiation states induced by the knockdown of Rnd2/Prag1/Fyn. Here, we showed that signaling through Rnd2/Prag1/Fyn is involved in the regulation of oligodendroglial cell-like morphological differentiation. The effects of knocking down the signaling cascade molecule can be recovered by hesperetin, highlighting an important molecular structure involved in morphological differentiation.

5

Sawaguchi, Sui, Rimi Suzuki, Hiroaki Oizumi, Katsuya Ohbuchi, Kazushige Mizoguchi, Masahiro Yamamoto, Yuki Miyamoto, and 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 (February 16, 2022): 212–44. http://dx.doi.org/10.3390/neurolint14010018.

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POLR3B and POLR3A are the major subunits of RNA polymerase III, which synthesizes non-coding RNAs such as tRNAs and rRNAs. Nucleotide mutations of the RNA polymerase 3 subunit b (polr3b) gene are responsible for hypomyelinating leukodystrophy 8 (HLD8), which is an autosomal recessive oligodendroglial cell disease. Despite the important association between POLR3B mutation and HLD8, it remains unclear how mutated POLR3B proteins cause oligodendroglial cell abnormalities. Herein, we show that a severe HLD8-associated nonsense mutation (Arg550-to-Ter (R550X)) primarily localizes POLR3B proteins as protein aggregates into lysosomes in the FBD-102b cell line as an oligodendroglial precursor cell model. Conversely, wild type POLR3B proteins were not localized in lysosomes. Additionally, the expression of proteins with the R550X mutation in cells decreased lysosome-related signaling through the mechanistic target of rapamycin (mTOR). Cells harboring the mutant constructs did not exhibit oligodendroglial cell differentiated phenotypes, which have widespread membranes that extend from their cell body. However, cells harboring the wild type constructs exhibited differentiated phenotypes. Ibuprofen, which is a non-steroidal anti-inflammatory drug (NSAID), improved the defects in their differentiation phenotypes and signaling through mTOR. These results indicate that the HLD8-associated POLR3B proteins with the R550X mutation are localized in lysosomes, decrease mTOR signaling, and inhibit oligodendroglial cell morphological differentiation, and ibuprofen improves these cellular pathological effects. These findings may reveal some of the molecular and cellular pathological mechanisms underlying HLD8 and their amelioration.

6

Issa, Y., D. C. Watts, A. J. Duxbury, P. A. Brunton, M. B. Watson, and C. M. Waters. "Mercuric chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13." Biomaterials 24, no. 6 (March 2003): 981–87. http://dx.doi.org/10.1016/s0142-9612(02)00436-2.

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7

Naffaa, Vanessa, Isabelle Hochar, Chéryane Lama, Romain Magny, Anne Regazzetti, Pierre Gressens, Olivier Laprévote, Nicolas Auzeil, and Anne-Laure Schang. "Bisphenol A Impairs Lipid Remodeling Accompanying Cell Differentiation in the Oligodendroglial Cell Line Oli-Neu." Molecules 27, no. 7 (March 31, 2022): 2274. http://dx.doi.org/10.3390/molecules27072274.

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In the central nervous system, the process of myelination involves oligodendrocytes that wrap myelin around axons. Myelin sheaths are mainly composed of lipids and ensure efficient conduction of action potentials. Oligodendrocyte differentiation is an essential preliminary step to myelination which, in turn, is a key event of neurodevelopment. Bisphenol A (BPA), a ubiquitous endocrine disruptor, is suspected to disrupt this developmental process and may, thus, contribute to several neurodevelopmental disorders. In this study, we assessed the effect of BPA on oligodendrocyte differentiation through a comprehensive analysis of cell lipidome by UHPLC-HRMS. For this purpose, we exposed the oligodendroglial cell line Oli-neu to several BPA concentrations for 72 h of proliferation and another 72 h of differentiation. In unexposed cells, significant changes occurred in lipid distribution during Oli-neu differentiation, including an increase in characteristic myelin lipids, sulfatides, and ethanolamine plasmalogens, and a marked remodeling of phospholipid subclasses and fatty acid contents. Moreover, BPA induced a decrease in sulfatide and phosphatidylinositol plasmalogen contents and modified monounsaturated/polyunsaturated fatty acid relative contents in phospholipids. These effects counteracted the lipid remodeling accompanying differentiation and were confirmed by gene expression changes. Altogether, our results suggest that BPA disrupts lipid remodeling accompanying early oligodendrocyte differentiation.

8

Torii, Tomohiro, Remina Shirai, Risa Kiminami, Satoshi Nishino, Takanari Sato, Sui Sawaguchi, Nana Fukushima, Yoichi Seki, Yuki Miyamoto, and Junji Yamauchi. "Hypomyelinating Leukodystrophy 10 (HLD10)-Associated Mutations of PYCR2 Form Large Size Mitochondria, Inhibiting Oligodendroglial Cell Morphological Differentiation." Neurology International 14, no. 4 (December 16, 2022): 1062–80. http://dx.doi.org/10.3390/neurolint14040085.

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Hypomyelinating leukodystrophy 10 (HLD10) is an autosomal recessive disease related to myelin sheaths in the central nervous system (CNS). In the CNS, myelin sheaths are derived from differentiated plasma membranes of oligodendrocytes (oligodendroglial cells) and surround neuronal axons to achieve neuronal functions. Nucleotide mutations of the pyrroline-5-carboxylate reductase 2 (PYCR2) gene are associated with HLD10, likely due to PYCR2’s loss-of-function. PYCR2 is a mitochondrial residential protein and catalyzes pyrroline-5-carboxylate to an amino acid proline. Here, we describe how each of the HLD10-associated missense mutations, Arg119-to-Cys [R119C] and Arg251-to-Cys [R251C], lead to forming large size mitochondria in the FBD-102b cell line, which is used as an oligodendroglial cell differentiation model. In contrast, the wild type proteins did not participate in the formation of large size mitochondria. Expression of each of the mutated R119C and R251C proteins in cells increased the fusion abilities in mitochondria and decreased their fission abilities relatively. The respective mutant proteins, but not wild type proteins also decreased the activities of mitochondria. While cells expressing the wild type proteins exhibited differentiated phenotypes with widespread membranes and increased expression levels of differentiation marker proteins following the induction of differentiation, cells harboring each of the mutant proteins did not. Taken together, these results indicate that an HLD10-associated PYCR2 mutation leads to the formation of large mitochondria with decreased activities, inhibiting oligodendroglial cell morphological differentiation. These results may reveal some of the pathological mechanisms in oligodendroglial cells underlying HLD10 at the molecular and cellular levels.

9

Bello-Morales, Raquel, Marta Pérez-Hernández, María Teresa Rejas, Fuencisla Matesanz, Antonio Alcina, and José Antonio López-Guerrero. "Interaction of PLP with GFP-MAL2 in the Human Oligodendroglial Cell Line HOG." PLoS ONE 6, no. 5 (May 9, 2011): e19388. http://dx.doi.org/10.1371/journal.pone.0019388.

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10

Craighead, Mark, Jessica Pole, and Catherine Waters. "Caspases mediate C2-ceramide-induced apoptosis of the human oligodendroglial cell line, MO3.13." Neuroscience Letters 278, no. 3 (January 2000): 125–28. http://dx.doi.org/10.1016/s0304-3940(99)00866-6.

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11

Studzinski, Diane M., Rose E. Callahan, and Joyce A. Benjamins. "Increased intracellular calcium alters myelin gene expression in the N20.1 oligodendroglial cell line." Journal of Neuroscience Research 57, no. 5 (August 25, 1999): 633–42. http://dx.doi.org/10.1002/(sici)1097-4547(19990901)57:5<633::aid-jnr5>3.0.co;2-i.

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12

Mancuso, Roberta, Simone Agostini, Ivana Marventano, Ambra Hernis, Marina Saresella, and Mario Clerici. "NCAM1 is the Target of miRNA-572: Validation in the Human Oligodendroglial Cell Line." Cellular and Molecular Neurobiology 38, no. 2 (March 22, 2017): 431–40. http://dx.doi.org/10.1007/s10571-017-0486-0.

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13

Horiuchi, Makoto, and Yasuhiro Tomooka. "An oligodendroglial progenitor cell line FBD-102b possibly secretes a radial glia-inducing factor." Neuroscience Research 56, no. 2 (October 2006): 213–19. http://dx.doi.org/10.1016/j.neures.2006.06.007.

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14

Bello-Morales, Raquel, María Fedetz, Antonio Alcina, Enrique Tabarés, and José Antonio López-Guerrero. "High susceptibility of a human oligodendroglial cell line to herpes simplex type 1 infection." Journal of Neurovirology 11, no. 2 (January 2005): 190–98. http://dx.doi.org/10.1080/13550280590924179.

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15

Bender, Herdis, Ziyuan Wang, Norbert Schuster, and Kerstin Krieglstein. "TIEG1 facilitates transforming growth factor-?-mediated apoptosis in the oligodendroglial cell line OLI-neu." Journal of Neuroscience Research 75, no. 3 (2004): 344–52. http://dx.doi.org/10.1002/jnr.10856.

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16

Matsumoto, Naoto, Yuki Miyamoto, Kohei Hattori, Akihiro Ito, Hironori Harada, Hiroaki Oizumi, Katsuya Ohbuchi, Kazushige Mizoguchi, and Junji Yamauchi. "PP1C and PP2A are p70S6K Phosphatases Whose Inhibition Ameliorates HLD12-Associated Inhibition of Oligodendroglial Cell Morphological Differentiation." Biomedicines 8, no. 4 (April 16, 2020): 89. http://dx.doi.org/10.3390/biomedicines8040089.

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Myelin sheaths created by oligodendroglial cells encase neuronal axons to achieve saltatory conduction and protect axons. Pelizaeus-Merzbacher disease (PMD) is a prototypic, hereditary demyelinating oligodendroglial disease of the central nervous system (CNS), and is currently known as hypomyelinating leukodystrophy 1 (HLD1). HLD12 is an autosomal recessive disorder responsible for the gene that encodes vacuolar protein sorting-associated protein 11 homolog (VPS11). VPS11 is a member of the molecular group controlling the early endosome antigen 1 (EEA1)- and Rab7-positive vesicle-mediated protein trafficking to the lysosomal compartments. Herein, we show that the HLD12-associated Cys846-to-Gly (C846G) mutation of VPS11 leads to its aggregate formation with downregulated signaling through 70 kDa S6 protein kinase (p70S6K) in the oligodendroglial cell line FBD-102b as the model. In contrast, wild-type proteins are localized in both EEA1- and Rab7-positive vesicles. Cells harboring the C846G mutant constructs decrease differentiated phenotypes with web-like structures following differentiation, whereas parental cells exhibit them suitably. It is of note that we identify PP1C and PP2A as the protein phosphatases for phosphorylated Thr-389 of p70S6K essential for kinase activation in cells. The respective knockdown experiments or inhibitor treatment stimulates phosphorylation of p70S6K and ameliorates the inhibition of morphological differentiation, as well as the formation of protein aggregates. These results indicate that inhibition of p70S6K phosphatases PP1C and PP2A improves the defective morphological differentiation associated with HLD12 mutation, thereby hinting at amelioration based on a possible molecular and cellular pathological mechanism underlying HLD12.

17

Murphy, Eric J., and Lloyd A. Horrocks. "Composition of the phospholipids and their fatty acids in the ROC-1 oligodendroglial cell line." Lipids 28, no. 1 (January 1993): 67–71. http://dx.doi.org/10.1007/bf02536364.

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18

Uezono, Yasuhito, Izumi Shibuya, Yoko Ueda, Keiko Tanaka, Yosuke Oishi, Nobuyuki Yanagihara, Susumu Ueno, et al. "Adrenomedullin increases intracellular Ca2+ and inositol 1,4,5-trisphosphate in human oligodendroglial cell line KG-1C." Brain Research 786, no. 1-2 (March 1998): 230–34. http://dx.doi.org/10.1016/s0006-8993(97)01430-3.

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19

Studzinski, Diane M., and Joyce A. Benjamins. "Cyclic AMP differentiation of the oligodendroglial cell line N20.1 switches staurosporine-induced cell death from necrosis to apoptosis." Journal of Neuroscience Research 66, no. 4 (2001): 691–97. http://dx.doi.org/10.1002/jnr.10003.

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20

Yoshioka, Akira, Yoko Yamaya, Shinji Saiki, Masumi Kanemoto, Genjiro Hirose, and David Pleasure. "Cyclic GMP/Cyclic GMP-Dependent Protein Kinase System Prevents Excitotoxicity in an Immortalized Oligodendroglial Cell Line." Journal of Neurochemistry 74, no. 2 (December 25, 2001): 633–40. http://dx.doi.org/10.1046/j.1471-4159.2000.740633.x.

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21

Solly, S. K., P. Daubas, M. Monge, A. Dautigny, and B. Zalc. "Functional Analysis of the Mouse Myelin/Oligodendrocyte Glycoprotein Gene Promoter in the Oligodendroglial CG4 Cell Line." Journal of Neurochemistry 68, no. 4 (November 18, 2002): 1705–11. http://dx.doi.org/10.1046/j.1471-4159.1997.68041705.x.

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22

Dominicis, Alessandra, Alice Del Giovane, Matteo Torreggiani, Antonella Damiana Recchia, Fabio Ciccarone, Maria Rosa Ciriolo, and Antonella Ragnini-Wilson. "N-Acetylaspartate Drives Oligodendroglial Differentiation via Histone Deacetylase Activation." Cells 12, no. 14 (July 14, 2023): 1861. http://dx.doi.org/10.3390/cells12141861.

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An unmet clinical goal in demyelinating pathologies is to restore the myelin sheath prior to neural degeneration. N-acetylaspartate (NAA) is an acetylated derivative form of aspartate, abundant in the healthy brain but severely reduced during traumatic brain injury and in patients with neurodegenerative pathologies. How extracellular NAA variations impact the remyelination process and, thereby, the ability of oligodendrocytes to remyelinate axons remains unexplored. Here, we evaluated the remyelination properties of the oligodendroglial (OL) mouse cell line Oli-neuM under different concentrations of NAA using a combination of biochemical, qPCR, immunofluorescence assays, and in vitro engagement tests, at NAA doses compatible with those observed in healthy brains and during brain injury. We observed that oligodendroglia cells respond to decreasing levels of NAA by stimulating differentiation and promoting gene expression of myelin proteins in a temporally regulated manner. Low doses of NAA potently stimulate Oli-neuM to engage with synthetic axons. Furthermore, we show a concentration-dependent expression of specific histone deacetylases essential for MBP gene expression under NAA or Clobetasol treatment. These data are consistent with the idea that oligodendrocytes respond to lowering the NAA concentration by activating the remyelination process via deacetylase activation.

23

Zhan, Jiangshan, Yuanxu Gao, Leo Heinig, Malena Beecken, Yangbo Huo, Wansong Zhang, Pingzhang Wang, et al. "Loss of the Novel Myelin Protein CMTM5 in Multiple Sclerosis Lesions and Its Involvement in Oligodendroglial Stress Responses." Cells 12, no. 16 (August 17, 2023): 2085. http://dx.doi.org/10.3390/cells12162085.

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This study comprehensively addresses the involvement of the protein CKLF-like Marvel transmembrane domain-containing family member 5 (CMTM5) in the context of demyelination and cytodegenerative autoimmune diseases, particularly multiple Sclerosis (MS). An observed reduction in CMTM5 expression in post-mortem MS lesions prompted further investigations in both in vitro and in vivo animal models. In the cuprizone animal model, we detected a decrease in CMTM5 expression in oligodendrocytes that is absent in other members of the CMTM protein family. Our findings also confirm these results in the experimental autoimmune encephalomyelitis (EAE) model with decreased CMTM5 expression in both cerebellum and spinal cord white matter. We also examined the effects of a Cmtm5 knockdown in vitro in the oligodendroglial Oli-neu mouse cell line using the CRISPR interference technique. Interestingly, we found no effects on cell response to thapsigargin-induced endoplasmic reticulum (ER) stress as determined by Atf4 activity, an indicator of cellular stress responses. Overall, these results substantiate previous findings suggesting that CMTM5, rather than contributing to myelin biogenesis, is involved in maintaining axonal integrity. Our study further demonstrates that the knockdown of Cmtm5 in vitro does not modulate oligodendroglial responses to ER stress. These results warrant further investigation into the functional role of CMTM5 during axonal degeneration in the context of demyelinating conditions.

24

Craighead, Mark W., Priyanka Tiwari, Robert G. Keynes, and Catherine M. Waters. "Human oligodendroglial cell line, MO3.13, can be protected from apoptosis using the general caspase inhibitor zVAD-FMK." Journal of Neuroscience Research 57, no. 2 (July 8, 1999): 236–43. http://dx.doi.org/10.1002/(sici)1097-4547(19990715)57:2<236::aid-jnr9>3.0.co;2-d.

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25

Praena, Beatriz, Raquel Bello-Morales, and José Antonio López-Guerrero. "Hsv-1 Endocytic Entry into a Human Oligodendrocytic Cell Line Is Mediated by Clathrin and Dynamin but Not Caveolin." Viruses 12, no. 7 (July 7, 2020): 734. http://dx.doi.org/10.3390/v12070734.

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Endocytosis is a pathway used by viruses to enter cells that can be classified based on the proteins involved, such as dynamin, clathrin or caveolin. Although the entry of herpes simplex type 1 (HSV-1) by endocytosis has been documented in different cell types, its dependence on clathrin has not been described whereas its dependence on dynamin has been shown according to the cell line used. The present work shows how clathrin-mediated endocytosis (CME) is one way that HSV-1 infects the human oligodendroglial (HOG) cell line. Partial dynamin inhibition using dynasore revealed a relationship between decrease of infection and dynamin inhibition, measured by viral titration and immunoblot. Co-localization between dynamin and HSV-1 was verified by immunofluorescence at the moment of viral entry into the cell. Inhibition by chlorpromazine revealed that viral progeny also decreased when clathrin was partially inhibited in our cell line. RT-qPCR of immediately early viral genes, specific entry assays and electron microscopy all confirmed clathrin’s participation in HSV-1 entry into HOG cells. In contrast, caveolin entry assays showed no effect on the entry of this virus. Therefore, our results suggest the participation of dynamin and clathrin during endocytosis of HSV-1 in HOG cells.

26

Uezono, Yasuhito, Ei-ichiro Nakamura, Yoko Ueda, Izumi Shibuya, Yoichi Ueta, Hiroki Yokoo, Toshihiko Yanagita, et al. "Production of cAMP by adrenomedullin in human oligodendroglial cell line KG1C: comparison with calcitonin gene-related peptide and amylin." Molecular Brain Research 97, no. 1 (December 2001): 59–69. http://dx.doi.org/10.1016/s0169-328x(01)00288-1.

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27

Rose, Lynn M., Susanne L. Jackevicius, and Edward A. Clark. "Monoclonal antibodies to human CD4, HNK-1, and LFA-1 surface antigens label the human oligodendroglial cell line KG-1." Journal of Neuroimmunology 16, no. 1 (September 1987): 147. http://dx.doi.org/10.1016/0165-5728(87)90358-4.

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28

Schuster, Norbert, Herdis Bender, Oliver G. Rössler, Anja Philippi, Nicole Dünker, Gerald Thiel, and Kerstin Krieglstein. "Transforming growth factor-β and tumor necrosis factor-α cooperate to induce apoptosis in the oligodendroglial cell line OLI-neu." Journal of Neuroscience Research 73, no. 3 (June 18, 2003): 324–33. http://dx.doi.org/10.1002/jnr.10666.

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29

Damato, Marina, Tristan Cardon, Maxence Wisztorski, Isabelle Fournier, Damiana Pieragostino, Ilaria Cicalini, Michel Salzet, Daniele Vergara, and Michele Maffia. "Protein Kinase C Activation Drives a Differentiation Program in an Oligodendroglial Precursor Model through the Modulation of Specific Biological Networks." International Journal of Molecular Sciences 22, no. 10 (May 15, 2021): 5245. http://dx.doi.org/10.3390/ijms22105245.

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Protein kinase C (PKC) activation induces cellular reprogramming and differentiation in various cell models. Although many effectors of PKC physiological actions have been elucidated, the molecular mechanisms regulating oligodendrocyte differentiation after PKC activation are still unclear. Here, we applied a liquid chromatography–mass spectrometry (LC–MS/MS) approach to provide a comprehensive analysis of the proteome expression changes in the MO3.13 oligodendroglial cell line after PKC activation. Our findings suggest that multiple networks that communicate and coordinate with each other may finally determine the fate of MO3.13 cells, thus identifying a modular and functional biological structure. In this work, we provide a detailed description of these networks and their participating components and interactions. Such assembly allows perturbing each module, thus describing its physiological significance in the differentiation program. We applied this approach by targeting the Rho-associated protein kinase (ROCK) in PKC-activated cells. Overall, our findings provide a resource for elucidating the PKC-mediated network modules that contribute to a more robust knowledge of the molecular dynamics leading to this cell fate transition.

30

Holzknecht, Christian, and Claudia Röhl. "Effects of Methylprednisolone and Glatiramer Acetate on Nitric Oxide Formation of Cytokine-Stimulated Cells from the Rat Oligodendroglial Cell Line OLN-93." Neuroimmunomodulation 17, no. 1 (2010): 23–30. http://dx.doi.org/10.1159/000243082.

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31

Martínez-Pinilla, Eva, Núria Rubio-Sardón, Rafael Peláez, Enrique García-Álvarez, Eva del Valle, Jorge Tolivia, Ignacio M. Larráyoz, and Ana Navarro. "Neuroprotective Effect of Apolipoprotein D in Cuprizone-Induced Cell Line Models: A Potential Therapeutic Approach for Multiple Sclerosis and Demyelinating Diseases." International Journal of Molecular Sciences 22, no. 3 (January 27, 2021): 1260. http://dx.doi.org/10.3390/ijms22031260.

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Apolipoprotein D (Apo D) overexpression is a general finding across neurodegenerative conditions so the role of this apolipoprotein in various neuropathologies such as multiple sclerosis (MS) has aroused a great interest in last years. However, its mode of action, as a promising compound for the development of neuroprotective drugs, is unknown. The aim of this work was to address the potential of Apo D to prevent the action of cuprizone (CPZ), a toxin widely used for developing MS models, in oligodendroglial and neuroblastoma cell lines. On one hand, immunocytochemical quantifications and gene expression measures showed that CPZ compromised neural mitochondrial metabolism but did not induce the expression of Apo D, except in extremely high doses in neurons. On the other hand, assays of neuroprotection demonstrated that antipsychotic drug, clozapine, induced an increase in Apo D synthesis only in the presence of CPZ, at the same time that prevented the loss of viability caused by the toxin. The effect of the exogenous addition of human Apo D, once internalized, was also able to directly revert the loss of cell viability caused by treatment with CPZ by a reactive oxygen species (ROS)-independent mechanism of action. Taken together, our results suggest that increasing Apo D levels, in an endo- or exogenous way, moderately prevents the neurotoxic effect of CPZ in a cell model that seems to replicate some features of MS which would open new avenues in the development of interventions to afford MS-related neuroprotection.

32

Fatatis, Alessandro, and Richard J. Miller. "Platelet-derived Growth Factor (PDGF)-induced Ca2+Signaling in the CG4 Oligodendroglial Cell Line and in Transformed Oligodendrocytes Expressing the β-PDGF Receptor." Journal of Biological Chemistry 272, no. 7 (February 14, 1997): 4351–58. http://dx.doi.org/10.1074/jbc.272.7.4351.

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33

Feng, Tuancheng, Rory R. Sheng, Santiago Solé-Domènech, Mohammed Ullah, Xiaolai Zhou, Christina S. Mendoza, Laura Camila Martinez Enriquez, et al. "A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination." Brain 143, no. 7 (June 23, 2020): 2255–71. http://dx.doi.org/10.1093/brain/awaa154.

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Abstract TMEM106B encodes a lysosomal membrane protein and was initially identified as a risk factor for frontotemporal lobar degeneration. Recently, a dominant D252N mutation in TMEM106B was shown to cause hypomyelinating leukodystrophy. However, how TMEM106B regulates myelination is still unclear. Here we show that TMEM106B is expressed and localized to the lysosome compartment in oligodendrocytes. TMEM106B deficiency in mice results in myelination defects with a significant reduction of protein levels of proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), the membrane proteins found in the myelin sheath. The levels of many lysosome proteins are significantly decreased in the TMEM106B-deficient Oli-neu oligodendroglial precursor cell line. TMEM106B physically interacts with the lysosomal protease cathepsin D and is required to maintain proper cathepsin D levels in oligodendrocytes. Furthermore, we found that TMEM106B deficiency results in lysosome clustering in the perinuclear region and a decrease in lysosome exocytosis and cell surface PLP levels. Moreover, we found that the D252N mutation abolished lysosome enlargement and lysosome acidification induced by wild-type TMEM106B overexpression. Instead, it stimulates lysosome clustering near the nucleus as seen in TMEM106B-deficient cells. Our results support that TMEM106B regulates myelination through modulation of lysosome function in oligodendrocytes.

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FIERZ, W., K. HEININGER, B. SCHAEFER, K. V. TOYKA, C. LININGTON, and H. LASSMANN. "Synergism in the Pathogenesis of EAE Induced by an MBP-Specific T-Cell Line and Monoclonal Antibodies to Galactocerebroside or a Myelin Oligodendroglial Glycoprotein." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (November 1988): 360–63. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27099.x.

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Blaschuk, K. L., E. E. Frost, and C. ffrench-Constant. "The regulation of proliferation and differentiation in oligodendrocyte progenitor cells by alphaV integrins." Development 127, no. 9 (May 1, 2000): 1961–69. http://dx.doi.org/10.1242/dev.127.9.1961.

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We have previously shown that oligodendrocyte progenitor cells exhibit developmental switching between alphav-associated beta integrin subunits to sequentially express alphavbeta1, alphavbeta3 and alphavbeta5 integrins during differentiation in vitro. To understand the role that alphavveta3 integrin may play in regulating oligodendrocyte progenitor cell behaviour, cells of the rat cell line, CG-4, were genetically engineered to constitutively express alphavbeta3 integrin by transfection with full-length human beta3 integrin subunit cDNA. Time-lapse videomicroscopy showed no effect of beta3 expression on cell migration but revealed enhanced proliferation on vitronectin substrata. Comparison of mitotic indices, as measured by 5-bromo-2′-deoxyuridine incorporation, confirmed that human beta3 integrin-expressing cells exhibited enhanced proliferation, as compared to both vector-only transfected, and wild-type CG-4 cells when switched to differentiation medium from growth medium, but only in cultures grown on vitronectin and not on poly-D-lysine. The effects on proliferation were inhibited by a function-blocking antibody specifically directed against the human beta3 integrin subunit. Human beta3 integrin-expressing cells also exhibited reduced differentiation. This differentiation could be reduced still further by a function-blocking monoclonal antibody against alphavbeta5 integrin, as could differentiation in the wild-type CG-4 cells. Taken together, these results suggest that alphavbeta3 integrin may regulate oligodendroglial cell proliferation and that both downregulation of alphavbeta3 integrin expression and signalling through alphavbeta5 integrin may be critical to continued differentiation in vitro.

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Nevin, M., X. Song, S. Japoni, J. Zagozewski, Q. Jiang, O. Becher, R. Godbout, DA Underhill, and DD Eisenstat. "09 Could DLX2 regulation of neural progenitor cell fate contribute to differentiation of diffuse intrinsic pontine glioma (DIPG)?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (June 2018): S16. http://dx.doi.org/10.1017/cjn.2018.305.

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Introduction: Diffuse intrinsic pontine glioma (DIPG) is refractory to therapy. The identification of histone H3.1/H3.3 K27M mutations in most DIPG has provided new insights. The DLX homeobox genes are expressed in the developing forebrain. The Dlx1/Dlx2 double knockout (DKO) mouse loses tangential GABAergic interneuron migration to the neocortex. We have identified genes that encode glutamic acid decarboxylase (GAD) enzymes as direct targets of DLX1/DLX2. In DIPG patients with H3.3 K27M mutations there is decreased Dlx2 and increased expression of the myelin transcription factor, Myt1. Methods and Results: We used bioinformatics approaches and chromatin immunoprecipitation (ChIP) assays to identify Olig2, Nkx2.2 and Myt1 promoter sequences as candidate DLX2 targets in vivo. DNA binding specificity was confirmed. The functional consequences of Dlx2 co-expression with reporter constructs of ChIP-isolated promoter fragments of Olig2 and Nkx2.2 demonstrated repression of gene targets in vitro. qPCR showed increased Olig2 and Nkx2.2 expression in the DKO forebrain. Stable transfection of a murine DIPG cell line with Dlx2 resulted in increased Gad1 and Gad2 and decreased Olig2 and Nkx2.2 expression. Of significance, we demonstrated decreased expression of H3.3 K27M and restoration of H3.3 K27 tri-methylation (me3). Conclusions: DLX transcription factors promote GABAergic interneuron and concomitant inhibition of oligodendroglial differentiation in neural progenitors by repression of a suite of genes including Olig2 and Nkx2.2. Restoration of H3 K27me3 expression in DIPG provides a promising lead towards exploration of differentiation as a therapeutic strategy for DIPG.

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Alotaibi, Lena, and Amal Alqasmi. "Identification of a de novo Mutation in TMEM106B in a Saudi Child Causes Hypomyelination Leukodystrophy." Global Medical Genetics 10, no. 01 (January 2023): 038–41. http://dx.doi.org/10.1055/s-0043-1764370.

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AbstractHypomyelinating leukodystrophies are one of the white matter disorders caused by a lack of myelin deposition in the central nervous system (CNS). Here, we report the first case of hypomyelinating leukodystrophy in the Middle East and Saudi Arabia. This condition is caused by a mutation in the TMEM106B gene (HLD16; MIM 617964). Hypotonia, congenital nystagmus, delayed motor development, and delayed speech are the main clinical manifestations. The affected patient has mild pyramidal syndrome, a mild intellectual disability, ataxic gait, hyperreflexia, intention tremor, dysmetria, and other motor difficulties. Findings from neuroimaging reveal severe, ongoing, and diffuse hypomyelination identified via the whole exome sequencing, a harmful missense mutation in the TMEM106B gene that is heterozygous. The patient is the offspring of two unrelated persons. The protein's cytoplasmic domain contains a variation that is located in highly conserved residues. In an oligodendroglial cell line, the mutant protein significantly lowered the mRNA production of important myelin genes, decreased branching, and increased cell mortality. TMEM106B is abundantly expressed in neurons and oligodendrocytes in the CNS and is localized in the late endosome and lysosome compartments. TMEM106B levels can be controlled at the transcriptional level through chromatin modification, at the mRNA level through miRNAs, and at the protein level through lysosomal functions. Our findings reveal a novel role of zinc homeostasis in oligodendrocyte development and myelin production and show that variations in TMEM163 induce hypomyelination leukodystrophy.

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Fierz, W., K. Heininger, B. Schaefer, K. V. Toyka, Ch Linington, and H. Lassmann. "Synergism in the pathogenesis of EAE induced by an MBP-specific T cell line and monoclonal antibodies to Galacto-Cerebroside or to a myelin oligodendroglial glycoprotein." Journal of Neuroimmunology 16, no. 1 (September 1987): 55–56. http://dx.doi.org/10.1016/0165-5728(87)90213-x.

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Rumsby, Martin, Keiko Ichihara-Tanaka, Terutoshi Kimura, Maria Scott, Laurie Haynes, and Takashi Muramatsu. "Bipolar undifferentiated CG-4 oligodendroglial line cells adhere, extend processes and disperse on midkine, a heparin-binding growth factor: orthovanadate and chondroitin sulphate E inhibit cell attachment." Neuroscience Research Communications 28, no. 1 (January 2001): 31–39. http://dx.doi.org/10.1002/1520-6769(200101/02)28:1<31::aid-nrc4>3.0.co;2-f.

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Silva, Maria Elena, Matías Hernández-Andrade, Nerea Abasolo, Cristóbal Espinoza-Cruells, Josselyne B. Mansilla, Carolina R. Reyes, Selena Aranda, et al. "DDR1 and Its Ligand, Collagen IV, Are Involved in In Vitro Oligodendrocyte Maturation." International Journal of Molecular Sciences 24, no. 2 (January 16, 2023): 1742. http://dx.doi.org/10.3390/ijms24021742.

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Discoidin domain receptor 1 (DDR1) is a tyrosine kinase receptor expressed in epithelial cells from different tissues in which collagen binding activates pleiotropic functions. In the brain, DDR1 is mainly expressed in oligodendrocytes (OLs), the function of which is unclear. Whether collagen can activate DDR1 in OLs has not been studied. Here, we assessed the expression of DDR1 during in vitro OL differentiation, including collagen IV incubation, and the capability of collagen IV to induce DDR1 phosphorylation. Experiments were performed using two in vitro models of OL differentiation: OLs derived from adult rat neural stem cells (NSCs) and the HOG16 human oligodendroglial cell line. Immunocytofluorescence, western blotting, and ELISA were performed to analyze these questions. The differentiation of OLs from NSCs was addressed using oligodendrocyte transcription factor 2 (Olig2) and myelin basic protein (MBP). In HOG16 OLs, collagen IV induced DDR1 phosphorylation through slow and sustained kinetics. In NSC-derived OLs, DDR1 was found in a high proportion of differentiating cells (MBP+/Olig2+), but its protein expression was decreased in later stages. The addition of collagen IV did not change the number of DDR1+/MBP+ cells but did accelerate OL branching. Here, we provide the first demonstration that collagen IV mediates the phosphorylation of DDR1 in HOG16 cells and that the in vitro co-expression of DDR1 and MBP is associated with accelerated branching during the differentiation of primary OLs.

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Glänzel, Nícolas Manzke, Belisa Parmeggiani, Mateus Grings, Bianca Seminotti, Morgana Brondani, Larissa D. Bobermin, César A. J. Ribeiro, André Quincozes-Santos, Jerry Vockley, and Guilhian Leipnitz. "Myelin Disruption, Neuroinflammation, and Oxidative Stress Induced by Sulfite in the Striatum of Rats Are Mitigated by the pan-PPAR agonist Bezafibrate." Cells 12, no. 12 (June 6, 2023): 1557. http://dx.doi.org/10.3390/cells12121557.

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Sulfite predominantly accumulates in the brain of patients with isolated sulfite oxidase (ISOD) and molybdenum cofactor (MoCD) deficiencies. Patients present with severe neurological symptoms and basal ganglia alterations, the pathophysiology of which is not fully established. Therapies are ineffective. To elucidate the pathomechanisms of ISOD and MoCD, we investigated the effects of intrastriatal administration of sulfite on myelin structure, neuroinflammation, and oxidative stress in rat striatum. Sulfite administration decreased FluoromyelinTM and myelin basic protein staining, suggesting myelin abnormalities. Sulfite also increased the staining of NG2, a protein marker of oligodendrocyte progenitor cells. In line with this, sulfite also reduced the viability of MO3.13 cells, which express oligodendroglial markers. Furthermore, sulfite altered the expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1), indicating neuroinflammation and redox homeostasis disturbances. Iba1 staining, another marker of neuroinflammation, was also increased by sulfite. These data suggest that myelin changes and neuroinflammation induced by sulfite contribute to the pathophysiology of ISOD and MoCD. Notably, post-treatment with bezafibrate (BEZ), a pan-PPAR agonist, mitigated alterations in myelin markers and Iba1 staining, and IL-1β, IL-6, iNOS and HO-1 expression in the striatum. MO3.13 cell viability decrease was further prevented. Moreover, pre-treatment with BEZ also attenuated some effects. These findings show the modulation of PPAR as a potential opportunity for therapeutic intervention in these disorders.

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Smith, Graham S. T., Lopamudra Homchaudhuri, Joan M. Boggs, and George Harauz. "Classic 18.5- and 21.5-kDa Myelin Basic Protein Isoforms Associate with Cytoskeletal and SH3-Domain Proteins in the Immortalized N19-Oligodendroglial Cell Line Stimulated by Phorbol Ester and IGF-1." Neurochemical Research 37, no. 6 (January 17, 2012): 1277–95. http://dx.doi.org/10.1007/s11064-011-0700-2.

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Agostini, Simone, Elisabetta Bolognesi, Roberta Mancuso, Ivana Marventano, Lorenzo Agostino Citterio, Franca Rosa Guerini, and Mario Clerici. "miR-23a-3p and miR-181a-5p modulate SNAP-25 expression." PLOS ONE 18, no. 1 (January 17, 2023): e0279961. http://dx.doi.org/10.1371/journal.pone.0279961.

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SNAP-25 protein is a key protein of the SNARE complex that is involved in synaptic vesicles fusion with plasma membranes and neurotransmitter release, playing a fundamental role in neural plasticity. Recently the concentration of three specific miRNAs–miR-27b-3p, miR-181a-5p and miR-23a-3p –was found to be associated with a specific SNAP-25 polymorphism (rs363050). in silico analysis showed that all the three miRNAs target SNAP-25, but the effect of the interaction between these miRNAs and the 3’UTR of SNAP-25 mRNA is currently unknown. For this reason, we verified in vitro whether miR-27b-3p, miR-181a-5p and miR-23a-3p modulate SNAP-25 gene and protein expression. Initial experiments using miRNAs-co-transfected Vero cells and SNAP-25 3’UTR luciferase reporter plasmids showed that miR-181a-5p (p≤0.01) and miR-23a-3p (p<0.05), but not miR-27b-3p, modulate the luciferase signal, indicating that these two miRNAs bind the SNAP-25 3’UTR. Results obtained using human oligodendroglial cell line (MO3.13) transfected with miR-181a-5p or miR-27b-3p confirmed that miR-181a-5p and miR-23a-3p regulate SNAP-25 gene and protein expression. Interestingly, the two miRNAs modulate in an opposite way SNAP-25, as miR-181a-5p significantly increases (p<0.0005), whereas miR-23a-3p decreases (p<0.0005) its expression. These results for the first time describe the ability of miR-181a-5p and miR-23a-3p to modulate SNAP-25 expression, suggesting their possible use as biomarkers or as therapeutical targets for diseases in which SNAP-25 expression is altered.

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Shahbandi, Ataollah, Saeid Atashpanjeh, Aileen Azari-Yam, Farideh Nejat, and Zohreh Habibi. "LINC-09. Coexisting glioneuronal tumor and adrenal ganglioneuroma." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i164. http://dx.doi.org/10.1093/neuonc/noac079.608.

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Abstract BACKGROUND: While both glial/glioneuronal neoplasia and ganglioneuroma have been reported as components of multiple primary neoplasms, no patient has been diagnosed with multiple primary neoplasms of cerebral glial/glioneuronal tumors with oligodendroglioma-like features and adrenal ganglioneuroma up to now. CASE: A previously healthy five-year-old girl was admitted with a two-week history of headaches and vomiting. Brain Magnetic resonance imaging (MRI) showed a massive heterogenous multi-cystic enhancing lesion in the right temporoparietal area with substantial vasogenic edema. The patient underwent craniotomy and tumor gross total resection. The intra-operative histomorphological assessment of the tumor was well-matched with a glial tumor. The patient developed systolic hypertension during postoperative care in the Intensive Care Unit. Subsequent abdominal CT scan unveiled a calcified mass of the left adrenal gland origin. Blood and urine catecholamine tests, vanillylmandelic acid (VMA), were within the normal range. The surgical excision specimen exhibited a clear cell neoplasm with diffuse infiltrative growth. A distinguishing combination of oligodendroglioma-like perinuclear haloes, clear cell appearance and vascular proliferation rendered the diffuse Glioneuronal tumor with Oligodendroglioma-like features. With the combination of oligodendroglial-like appearance, negative 1p/19q codeletion, Wild IDH, no BRAF mutation, weak GFAP, and positive synaptophysin altogether, the tumor was compatible with the novel diffuse glioneuronal tumor with oligodendroglioma-like features and nuclear clusters (DGONC). The patient underwent laparotomy and tumor resection subsequently. Morphologic histopathological examinations of the adrenal mass were in line with ganglioneuroma. After discharge, no pathological uptake was identified with iodine-131 meta-iodobenzylguanidine scan (MIBG scan). No tumor residue was apparent on postoperative brain MRI. The patient received no adjuvant therapy for brain and adrenal tumors and underwent close surveillance for both tumors. No clinical or radiologic recurrence was recognized after six months of follow-up. CONCLUSIONS: Concurrent glioneuronal tumor and ganglioneuroma can be managed safely when diagnosed timely, leading to favorable outcomes.

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Schaff, Lauren R., and Ingo K. Mellinghoff. "Glioblastoma and Other Primary Brain Malignancies in Adults." JAMA 329, no. 7 (February 21, 2023): 574. http://dx.doi.org/10.1001/jama.2023.0023.

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ImportanceMalignant primary brain tumors cause more than 15 000 deaths per year in the United States. The annual incidence of primary malignant brain tumors is approximately 7 per 100 000 individuals and increases with age. Five-year survival is approximately 36%.ObservationsApproximately 49% of malignant brain tumors are glioblastomas, and 30% are diffusely infiltrating lower-grade gliomas. Other malignant brain tumors include primary central nervous system (CNS) lymphoma (7%) and malignant forms of ependymomas (3%) and meningiomas (2%). Symptoms of malignant brain tumors include headache (50%), seizures (20%-50%), neurocognitive impairment (30%-40%), and focal neurologic deficits (10%-40%). Magnetic resonance imaging before and after a gadolinium-based contrast agent is the preferred imaging modality for evaluating brain tumors. Diagnosis requires tumor biopsy with consideration of histopathological and molecular characteristics. Treatment varies by tumor type and often includes a combination of surgery, chemotherapy, and radiation. For patients with glioblastoma, the combination of temozolomide with radiotherapy improved survival when compared with radiotherapy alone (2-year survival, 27.2% vs 10.9%; 5-year survival, 9.8% vs 1.9%; hazard ratio [HR], 0.6 [95% CI, 0.5-0.7]; P &lt; .001). In patients with anaplastic oligodendroglial tumors with 1p/19q codeletion, probable 20-year overall survival following radiotherapy without vs with the combination of procarbazine, lomustine, and vincristine was 13.6% vs 37.1% (80 patients; HR, 0.60 [95% CI, 0.35-1.03]; P = .06) in the EORTC 26951 trial and 14.9% vs 37% in the RTOG 9402 trial (125 patients; HR, 0.61 [95% CI, 0.40-0.94]; P = .02). Treatment of primary CNS lymphoma includes high-dose methotrexate-containing regimens, followed by consolidation therapy with myeloablative chemotherapy and autologous stem cell rescue, nonmyeloablative chemotherapy regimens, or whole brain radiation.Conclusions and RelevanceThe incidence of primary malignant brain tumors is approximately 7 per 100 000 individuals, and approximately 49% of primary malignant brain tumors are glioblastomas. Most patients die from progressive disease. First-line therapy for glioblastoma is surgery followed by radiation and the alkylating chemotherapeutic agent temozolomide.

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Chierto, Elena, Giulia Cristinziano, Francesca Sapone, Delphine Meffre, and Mehrnaz Jafarian-Tehrani. "ffect of Etazolate on ROS Production after tBHP-Induced Oxidative Stress in Oligodendroglial 158N Cell Line." Reactive Oxygen Species, 2020. http://dx.doi.org/10.20455/ros.2020.807.

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Kremp, Marco, Tim Aberle, Elisabeth Sock, Bettina Bohl, Simone Hillgärtner, Jürgen Winkler, and Michael Wegner. "Transcription factor Olig2 is a major downstream effector of histone demethylase Phf8 during oligodendroglial development." Glia, April 13, 2024. http://dx.doi.org/10.1002/glia.24538.

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AbstractThe plant homeodomain finger protein Phf8 is a histone demethylase implicated by mutation in mice and humans in neural crest defects and neurodevelopmental disturbances. Considering its widespread expression in cell types of the central nervous system, we set out to determine the role of Phf8 in oligodendroglial cells to clarify whether oligodendroglial defects are a possible contributing factor to Phf8‐dependent neurodevelopmental disorders. Using loss‐ and gain‐of‐function approaches in oligodendroglial cell lines and primary cell cultures, we show that Phf8 promotes the proliferation of rodent oligodendrocyte progenitor cells and impairs their differentiation to oligodendrocytes. Intriguingly, Phf8 has a strong positive impact on Olig2 expression by acting on several regulatory regions of the gene and changing their histone modification profile. Taking the influence of Olig2 levels on oligodendroglial proliferation and differentiation into account, Olig2 likely acts as an important downstream effector of Phf8 in these cells. In line with such an effector function, ectopic Olig2 expression in Phf8‐deficient cells rescues the proliferation defect. Additionally, generation of human oligodendrocytes from induced pluripotent stem cells did not require PHF8 in a system that relies on forced expression of Olig2 during oligodendroglial induction. We conclude that Phf8 may impact nervous system development at least in part through its action in oligodendroglial cells.

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Del Giovane, Alice, Mariagiovanna Russo, Linda Tirou, Hélène Faure, Martial Ruat, Sonia Balestri, Carola Sposato, et al. "Smoothened/AMP-Activated Protein Kinase Signaling in Oligodendroglial Cell Maturation." Frontiers in Cellular Neuroscience 15 (January 10, 2022). http://dx.doi.org/10.3389/fncel.2021.801704.

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The regeneration of myelin is known to restore axonal conduction velocity after a demyelinating event. Remyelination failure in the central nervous system contributes to the severity and progression of demyelinating diseases such as multiple sclerosis. Remyelination is controlled by many signaling pathways, such as the Sonic hedgehog (Shh) pathway, as shown by the canonical activation of its key effector Smoothened (Smo), which increases the proliferation of oligodendrocyte precursor cells via the upregulation of the transcription factor Gli1. On the other hand, the inhibition of Gli1 was also found to promote the recruitment of a subset of adult neural stem cells and their subsequent differentiation into oligodendrocytes. Since Smo is also able to transduce Shh signals via various non-canonical pathways such as the blockade of Gli1, we addressed the potential of non-canonical Smo signaling to contribute to oligodendroglial cell maturation in myelinating cells using the non-canonical Smo agonist GSA-10, which downregulates Gli1. Using the Oli-neuM cell line, we show that GSA-10 promotes Gli2 upregulation, MBP and MAL/OPALIN expression via Smo/AMP-activated Protein Kinase (AMPK) signaling, and efficiently increases the number of axonal contact/ensheathment for each oligodendroglial cell. Moreover, GSA-10 promotes the recruitment and differentiation of oligodendroglial progenitors into the demyelinated corpus callosum in vivo. Altogether, our data indicate that non-canonical signaling involving Smo/AMPK modulation and Gli1 downregulation promotes oligodendroglia maturation until axon engagement. Thus, GSA-10, by activation of this signaling pathway, represents a novel potential remyelinating agent.

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Bey, Guillermo Rodriguez, and Quasar Saleem Padiath. "Enhanced differentiation of the mouse oli-neu oligodendroglial cell line using optimized culture conditions." BMC Research Notes 16, no. 1 (August 4, 2023). http://dx.doi.org/10.1186/s13104-023-06432-w.

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Abstract Objective Oligodendrocytes (OL) are the glial cell type in the CNS that are responsible for myelin formation. The ability to culture OLs in vitro has provided critical insights into the mechanisms underlying their function. However, primary OL cultures are tedious to obtain, difficult to propagate and are not easily conducive to genetic manipulation. To overcome these obstacles, researchers have generated immortalized OL like cell lines derived from various species. One such cell line is the mouse Oli-neu line which is thought to recapitulate characteristics of OLs in early stages of maturity. They have been extensively utilized in multiple studies as surrogates for OLs, especially in analyzing epigenetic modifications and regulatory pathways in the OL lineage. Results In this report we present the development of optimized culture media and growth conditions that greatly facilitate the differentiation of Oli-neu cells. Oli-neu cells differentiated using these new protocols exhibit a higher expression of myelin related genes and increased branching, both of which are defining characteristics of mature OLs, when compared to previous culture protocols. We envision that these new culture conditions will greatly facilitate the use of Oli-neu cells and enhance their ability to recapitulate the salient features of primary OLs.

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Joerger-Messerli, Marianne S., Gierin Thomi, Valérie Haesler, Irene Keller, Patricia Renz, Daniel V. Surbek, and Andreina Schoeberlein. "Human Wharton’s Jelly Mesenchymal Stromal Cell-Derived Small Extracellular Vesicles Drive Oligodendroglial Maturation by Restraining MAPK/ERK and Notch Signaling Pathways." Frontiers in Cell and Developmental Biology 9 (March 23, 2021). http://dx.doi.org/10.3389/fcell.2021.622539.

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Peripartum cerebral hypoxia and ischemia, and intrauterine infection and inflammation, are detrimental for the precursor cells of the myelin-forming oligodendrocytes in the prematurely newborn, potentially leading to white matter injury (WMI) with long-term neurodevelopmental sequelae. Previous data show that hypomyelination observed in WMI is caused by arrested oligodendroglial maturation rather than oligodendrocyte-specific cell death. In a rat model of premature WMI, we have recently shown that small extracellular vesicles (sEV) derived from Wharton’s jelly mesenchymal stromal cells (WJ-MSC) protect from myelination deficits. Thus, we hypothesized that sEV derived from WJ-MSC directly promote oligodendroglial maturation in oligodendrocyte precursor cells. To test this assumption, sEV were isolated from culture supernatants of human WJ-MSC by ultracentrifugation and co-cultured with the human immortalized oligodendrocyte precursor cell line MO3.13. As many regulatory functions in WMI have been ascribed to microRNA (miR) and as sEV are carriers of functional miR which can be delivered to target cells, we characterized and quantified the miR content of WJ-MSC-derived sEV by next-generation sequencing. We found that WJ-MSC-derived sEV co-localized with MO3.13 cells within 4 h. After 5 days of co-culture, the expression of myelin basic protein (MBP), a marker for mature oligodendrocytes, was significantly increased, while the oligodendrocyte precursor marker platelet-derived growth factor alpha (PDGFRα) was decreased. Notch and MAPK/ERK pathways known to inhibit oligodendrocyte maturation and differentiation were significantly reduced. The pathway enrichment analysis showed that the miR present in WJ-MSC-derived sEV target genes having key roles in the MAPK pathway. Our data strongly suggest that sEV from WJ-MSC directly drive the maturation of oligodendrocyte precursor cells by repressing Notch and MAPK/ERK signaling.