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Glial responses during epileptogenesis in Mus musculus point to potential therapeutic targets

Kalozoumi, Georgia, Kel-Margoulis, Olga, Vafiadaki, Elizabeth, Greenberg, David, Bernard, Hélène, Soreq, Hermona, Depaulis, Antoine, Sanoudou, Despina·2018·PLOS ONE

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Fig 1 Electroencephalographic and histological consequences of kainate injection into the dorsal hippocampus in mice. A. EEG recordings performed at 6, 12 and 24h post-KA (n = 6), showing examples of EEG patterns recorded during the focal status epilepticus in the cortex (Cx) and injected hippocampus (Hipp). At 6 h post-KA there was no epileptiform activity in the cortex, whereas a discharge of spike and poly-spikes was observed in the hippocampus. At 12h, bursts of spikes were regularly observed in the hippocampus and ipsilateral cortex, whereas only occasional spikes were recorded in either the cortex or the hippocampus between 22 and 24h. B. Fluoro-jade B labeling 24h post-injection in saline-injected mouse (left) and KA-injected mouse (right), indicating the presence of injured cells in CA1, CA3 and hilus area. C. Nissl staining 24h post-injection in saline-injected mouse (left) and KA-injected mouse (right) indicating that most cells were pyknotic in CA1, CA3 and hilus area. Bar = 500 μm. * = track of the injection cannula.
Fig 1 Electroencephalographic and histological consequences of kainate injection into the dorsal hippocampus in mice. A. EEG recordings performed at 6, 12 and 24h post-KA (n = 6), showing examples of EEG patterns recorded during the focal status epilepticus in the cortex (Cx) and injected hippocampus (Hipp). At 6 h post-KA there was no epileptiform activity in the cortex, whereas a discharge of spike and poly-spikes was observed in the hippocampus. At 12h, bursts of spikes were regularly observed in the hippocampus and ipsilateral cortex, whereas only occasional spikes were recorded in either the cortex or the hippocampus between 22 and 24h. B. Fluoro-jade B labeling 24h post-injection in saline-injected mouse (left) and KA-injected mouse (right), indicating the presence of injured cells in CA1, CA3 and hilus area. C. Nissl staining 24h post-injection in saline-injected mouse (left) and KA-injected mouse (right) indicating that most cells were pyknotic in CA1, CA3 and hilus area. Bar = 500 μm. * = track of the injection cannula.CC BY · PubMed Central
Fig 2 Comparison of the significant transcript changes across 6, 12 and 24h post KA injection. Area-proportional Venn diagram with the number of significantly changed probe sets at each post-injection time point. A total of 54 animals were used (n = 9/time-point/treatment) for the microarray analysis, and SAM was applied for the analysis of KA- versus saline-injected hippocampi at each time point interrogated (thresholds: fold change ≥ |2|, FDR = 0%).
Fig 2 Comparison of the significant transcript changes across 6, 12 and 24h post KA injection. Area-proportional Venn diagram with the number of significantly changed probe sets at each post-injection time point. A total of 54 animals were used (n = 9/time-point/treatment) for the microarray analysis, and SAM was applied for the analysis of KA- versus saline-injected hippocampi at each time point interrogated (thresholds: fold change ≥ |2|, FDR = 0%).CC BY · PubMed Central
Fig 3 Schematic representation of the network of downstream molecules regulated by Cybb at 24h. The analysis was performed using the “Master regulators in networks (TRANSPATH®)” workflow (geneXplain 2.2 web edition) (thresholds: Score >0.2 and Z-Score >1), for all the significantly changed transcripts detected by microarrays in KA- versus saline-injected hippocampi at 24h (SAM analysis, thresholds: fold change > |2|, FDR = 0%, n = 9/time-point/treatment). Red: genes overexpressed at 24h, blue: genes not significantly changed, p: phosphorylation.
Fig 3 Schematic representation of the network of downstream molecules regulated by Cybb at 24h. The analysis was performed using the “Master regulators in networks (TRANSPATH®)” workflow (geneXplain 2.2 web edition) (thresholds: Score >0.2 and Z-Score >1), for all the significantly changed transcripts detected by microarrays in KA- versus saline-injected hippocampi at 24h (SAM analysis, thresholds: fold change > |2|, FDR = 0%, n = 9/time-point/treatment). Red: genes overexpressed at 24h, blue: genes not significantly changed, p: phosphorylation.CC BY · PubMed Central
Fig 4 Summary diagram of the key biological changes detected during epileptogenesis. At 6h multiple neuroexcitation-induced immediate and early response genes are significantly changed. At 12h specific ion conduction, neurotransmission, astrocyte/microglial activation, inflammation and apoptosis related mechanisms are significantly altered. Importantly, at 24h, the silent phase of epileptogenesis, Nox2 (Cybb) and Vim are predicted to act as upstream regulators of key biological processes ultimately leading to activated glia, NOX-mediated ROS, neuroinflammation and neurodegeneration. The presence or absence of KA-induced epileptiform activity is denoted with orange and white color, respectively. The spontaneous epileptiform activity is marked with blue color.
Fig 4 Summary diagram of the key biological changes detected during epileptogenesis. At 6h multiple neuroexcitation-induced immediate and early response genes are significantly changed. At 12h specific ion conduction, neurotransmission, astrocyte/microglial activation, inflammation and apoptosis related mechanisms are significantly altered. Importantly, at 24h, the silent phase of epileptogenesis, Nox2 (Cybb) and Vim are predicted to act as upstream regulators of key biological processes ultimately leading to activated glia, NOX-mediated ROS, neuroinflammation and neurodegeneration. The presence or absence of KA-induced epileptiform activity is denoted with orange and white color, respectively. The spontaneous epileptiform activity is marked with blue color.CC BY · PubMed Central

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Research works printed but not linked: 104

  1. F Cendes, 2011, Early childhood prolonged febrile convulsions, atrophy and sclerosis of mesial structures, and temporal lobe epilepsy: An MRI volumetric study, Neurology, 76, 1845, 10.1212/01.wnl.0000398451.98153.85 · DOI
  2. A Pitkänen, 2011, Mechanisms of epileptogenesis and potential treatment targets, The Lancet Neurology, 10, 173, 10.1016/S1474-4422(10)70310-0 · DOI
  3. GW Mathern, 1995, Influence of the type of initial precipitating injury and at what age it occurs on course and outcome in patients with temporal lobe seizures, J Neurosurg, 82, 220, 10.3171/jns.1995.82.2.0220 · DOI
  4. GW Mathern, 1996, The pathogenic and progressive features of chronic human hippocampal epilepsy, Epilepsy Research, 26, 151, 10.1016/S0920-1211(96)00052-6 · DOI
  5. J. Engel, 2001, Mesial temporal lobe epilepsy: what have we learned?, The Neuroscientist, 7, 340, 10.1177/107385840100700410 · DOI
  6. W Löscher, 2015, The enigma of the latent period in the development of symptomatic acquired epilepsy—Traditional view versus new concepts, Epilepsy Behav, 52, 78, 10.1016/j.yebeh.2015.08.037 · DOI
  7. JG Hunsberger, 2005, Gene profiling the response to kainic acid induced seizures, Molecular Brain Research, 141, 95, 10.1016/j.molbrainres.2005.08.005 · DOI
  8. AK Sharma, 2009, Kainic Acid-induced F-344 Rat model of Mesial Temporal Lobe Epilepsy: Gene Expression and Canonical Pathways, Toxicologic Pathology, 37, 776, 10.1177/0192623309344202 · DOI
  9. HB Laurén, 2010, Transcriptome Analysis of the Hippocampal CA1 Pyramidal Cell Region after Kainic Acid-Induced Status Epilepticus in Juvenile Rats, PLoS One, 5, e10733, 10.1371/journal.pone.0010733 · DOI
  10. OK Okamoto, 2010, Whole transcriptome analysis of the hippocampus: toward a molecular portrait of epileptogenesis, BMC Genomics, 11, 230, 10.1186/1471-2164-11-230 · DOI
  11. JA Gorter, 2006, Potential new antiepileptogenic targets indicated by microarray analysis in a rat model for temporal lobe epilepsy, The Journal of Neuroscience, 26, 11083, 10.1523/JNEUROSCI.2766-06.2006 · DOI · Paper page
  12. D Motti, 2010, Gene expression analysis of the emergence of epileptiform activity after focal injection of kainic acid into mouse hippocampus, European Journal of Neuroscience, 32, 1364, 10.1111/j.1460-9568.2010.07403.x · DOI
  13. AS Vieira, 2016, RNA sequencing reveals region- specific molecular mechanisms associated with epileptogenesis in a model of classical hippocampal sclerosis, Nature Publishing Group, 1
  14. YY Wang, 2010, Global Expression Profiling in Epileptogenesis: Does It Add to the Confusion?, Brain Pathology, 20, 1, 10.1111/j.1750-3639.2008.00254.x · DOI
  15. Y Ben-Ari, 1980, Injections of kainic acid into the amygdaloid complex of the rat: an electrographic, clinical and histological study in relation to the pathology of epilepsy, NSC, 5, 515
  16. I Guillemain, 2012, Animal models to study aetiopathology of epilepsy: what are the features to model?, Epileptic Disord, 14, 217, 10.1684/epd.2012.0528 · DOI
  17. V Bouilleret, 1999, Recurrent seizures and hippocampal sclerosis following intrahippocampal kainate injection in adult mice: electroencephalography, histopathology and synaptic reorganization similar to mesial temporal lobe epilepsy, NSC, 89, 717
  18. V Riban, 2002, Evolution of hippocampal epileptic activity during the development of hippocampal sclerosis in a mouse model of temporal lobe epilepsy, NSC, 112, 101
  19. R Meier, 2007, Short-term changes in bilateral hippocampal coherence precede epileptiform events, NeuroImage, 38, 138, 10.1016/j.neuroimage.2007.07.016 · DOI
  20. C Heinrich, 2011, Increase in BDNF-mediated TrkB signaling promotes epileptogenesis in a mouse model of mesial temporal lobe epilepsy, Neurobiology of Disease, 42, 35, 10.1016/j.nbd.2011.01.001 · DOI
  21. A Depaulis, 2015, Animal models for mesiotemporal lobe epilepsy: The end of a misunderstanding?, Revue Neurologique, 171, 217, 10.1016/j.neurol.2015.01.558 · DOI
  22. JE Kralic, 2005, Disruption of the neurogenic potential of the dentate gyrus in a mouse model of temporal lobe epilepsy with focal seizures, European Journal of Neuroscience, 22, 1916, 10.1111/j.1460-9568.2005.04386.x · DOI
  23. C Heinrich, 2006, Reelin Deficiency and Displacement of Mature Neurons, But Not Neurogenesis, Underlie the Formation of Granule Cell Dispersion in the Epileptic Hippocampus, The Journal of Neuroscience, 26, 4701, 10.1523/JNEUROSCI.5516-05.2006 · DOI
  24. T Dugladze, 2007, Impaired hippocampal rhythmogenesis in a mouse model of mesial temporal lobe epilepsy, Proc Natl Acad Sci USA, 104, 17530, 10.1073/pnas.0708301104 · DOI
  25. N Nitta, 2008, Granule cell dispersion develops without neurogenesis and does not fully depend on astroglial cell generation in a mouse model of temporal lobe epilepsy, Epilepsia, 49, 1711, 10.1111/j.1528-1167.2008.01595.x · DOI
  26. F Antonucci, 2008, Botulinum neurotoxin E (BoNT/E) reduces CA1 neuron loss and granule cell dispersion, with no effects on chronic seizures, in a mouse model of temporal lobe epilepsy, Experimental Neurology, 210, 388, 10.1016/j.expneurol.2007.11.012 · DOI
  27. M Maroso, 2010, Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures, Nature Medicine, 16, 413, 10.1038/nm.2127 · DOI · Paper page
  28. V Duveau, 2016, Differential Effects of Antiepileptic Drugs on Focal Seizures in the Intrahippocampal Kainate Mouse Model of Mesial Temporal Lobe Epilepsy, CNS Neurosci Ther, 22, 497, 10.1111/cns.12523 · DOI
  29. F Pernot, 2011, Inflammatory changes during epileptogenesis and spontaneous seizures in a mouse model of mesiotemporal lobe epilepsy, Epilepsia, 52, 2315, 10.1111/j.1528-1167.2011.03273.x · DOI
  30. D Sanoudou, 2003, Expression profiling reveals altered satellite cell numbers and glycolytic enzyme transcription in nemaline myopathy muscle, Proc Natl Acad Sci USA, 100, 4666, 10.1073/pnas.0330960100 · DOI
  31. A Tsompanidis, 2016, Ciliary neurotrophic factor upregulates follistatin and Pak1, causes overexpression of muscle differentiation related genes and downregulation of established atrophy mediators in skeletal muscle, Metabolism—Clinical and Experimental, 65, 915, 10.1016/j.metabol.2016.03.005 · DOI
  32. H Guo, 2010, 466, 835
  33. NP Tsai, 2009, MicroRNA mir-346 targets the 5′-untranslated region of receptor-interacting protein 140 (RIP140) mRNA and up-regulates its protein expression, Biochemical Journal
  34. F Suzuki, 2005, Glutamate receptor antagonists and benzodiazepine inhibit the progression of granule cell dispersion in a mouse model of mesial temporal lobe epilepsy, Epilepsia, 46, 193, 10.1111/j.0013-9580.2005.35504.x · DOI
  35. A Pitkänen, 2013, Issues related to development of antiepileptogenic therapies, Epilepsia, 54, 35, 10.1111/epi.12297 · DOI
  36. J Honkaniemi, 1999, Prolonged expression of zinc finger immediate-early gene mRNAs and decreased protein synthesis following kainic acid induced seizures, Eur J Neurosci, 11, 10, 10.1046/j.1460-9568.1999.00401.x · DOI
  37. KV Christensen, 2010, Levetiracetam attenuates hippocampal expression of synaptic plasticity-related immediate early and late response genes in amygdala-kindled rats, BMC Neurosci, 11, 9, 10.1186/1471-2202-11-9 · DOI
  38. K Akiyama, 2008, mRNA expression of activity-regulated cytoskeleton-associated protein (arc) in the amygdala-kindled rats, Brain Research, 1189, 236, 10.1016/j.brainres.2007.10.102 · DOI
  39. WK Nahm, 1998, Nonobligate role of early or sustained expression of immediate-early gene proteins c-fos, c-jun, and Zif/268 in hippocampal mossy fiber sprouting, Journal of Neuroscience, 18, 9245, 10.1523/JNEUROSCI.18-22-09245.1998 · DOI
  40. PJ Clark, 2011, Induction of c-Fos, Zif268, and Arc from acute bouts of voluntary wheel running in new and pre-existing adult mouse hippocampal granule neurons, Neuroscience, 184, 16, 10.1016/j.neuroscience.2011.03.072 · DOI
  41. Y Ji, 2010, 13, 302
  42. H Gerstein, 2012, Rescue of synaptic plasticity and spatial learning deficits in the hippocampus of Homer1 knockout mice by recombinant Adeno-associated viral gene delivery of Homer1c, Neurobiology of Learning and Memory, 97, 17, 10.1016/j.nlm.2011.08.009 · DOI
  43. V Bitsika, 2016, High-Throughput LC-MS/MS Proteomic Analysis of a Mouse Model of Mesiotemporal Lobe Epilepsy Predicts Microglial Activation Underlying Disease Development, J Proteome Res, 15, 1546, 10.1021/acs.jproteome.6b00003 · DOI
  44. J Choi, 2011, Translocator protein (18 kDa)/peripheral benzodiazepine receptor specific ligands induce microglia functions consistent with an activated state, Glia, 59, 219, 10.1002/glia.21091 · DOI
  45. AM Scarf, 2011, The translocator protein, Journal of Nuclear Medicine, 52, 677, 10.2967/jnumed.110.086629 · DOI
  46. Z Xu, 2011, Role of signal transducer and activator of transcription-3 in up-regulation of GFAP after epilepsy, Neurochemical Research, 36, 2208, 10.1007/s11064-011-0576-1 · DOI
  47. E Aronica, 2000, Upregulation of metabotropic glutamate receptor subtype mGluR3 and mGluR5 in reactive astrocytes in a rat model of mesial temporal lobe epilepsy, Eur J Neurosci, 12, 2333, 10.1046/j.1460-9568.2000.00131.x · DOI
  48. TL Sandhya, 1998, A light and electron microscopic study of cytoplasmic phospholipase A2 and cyclooxygenase-2 in the hippocampus after kainate lesions, Brain Research, 788, 223, 10.1016/S0006-8993(97)01552-7 · DOI
  49. AA Farooqui, 2004, Neuroprotection abilities of cytosolic phospholipase A2 inhibitors in kainic acid-induced neurodegeneration, Curr Drug Targets Cardiovasc Haematol Disord, 4, 85, 10.2174/1568006043481239 · DOI
  50. JR Sundaram, 2012, Cdk5/p25-induced cytosolic PLA2-mediated lysophosphatidylcholine production regulates neuroinflammation and triggers neurodegeneration, The Journal of Neuroscience, 32, 1020, 10.1523/JNEUROSCI.5177-11.2012 · DOI
  51. DK Kaushik, 2010, Krüppel-like factor 4, a novel transcription factor regulates microglial activation and subsequent neuroinflammation, Journal of Neuroinflammation, 7, 68, 10.1186/1742-2094-7-68 · DOI
  52. DK Kaushik, 2012, Therapeutic targeting of Krüppel-like factor 4 abrogates microglial activation, Journal of Neuroinflammation, 9, 57, 10.1186/1742-2094-9-57 · DOI
  53. Y Zhang, 2006, Interleukin-11 potentiates oligodendrocyte survival and maturation, and myelin formation, The Journal of Neuroscience, 26, 12174, 10.1523/JNEUROSCI.2289-06.2006 · DOI
  54. HM Mitchell, 2011, Cold pre‐conditioning neuroprotection depends on TNF‐α and is enhanced by blockade of interleukin‐11, Journal of …
  55. A Fahrner, 2007, Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients, Experimental Neurology, 203, 320, 10.1016/j.expneurol.2006.08.023 · DOI
  56. A Crespel, 2002, Immature-like astrocytes are associated with dentate granule cell migration in human temporal lobe epilepsy, Neuroscience Letters, 330, 114, 10.1016/S0304-3940(02)00718-8 · DOI
  57. GW Mathern, 1997, Granule cell mRNA levels for BDNF, NGF, and NT-3 correlate with neuron losses or supragranular mossy fiber sprouting in the chronically damaged and epileptic human hippocampus, Molecular and Chemical Neuropathology, 30, 53, 10.1007/BF02815150 · DOI
  58. NC de Lanerolle, 2005, New facets of the neuropathology and molecular profile of human temporal lobe epilepsy, Epilepsy Behav, 7, 190, 10.1016/j.yebeh.2005.06.003 · DOI
  59. A Vezzani, 2005, Brain inflammation in epilepsy: experimental and clinical evidence, Epilepsia, 46, 1724, 10.1111/j.1528-1167.2005.00298.x · DOI
  60. T Ravizza, 2011, Inflammation and prevention of epileptogenesis, Neuroscience Letters, 497, 223, 10.1016/j.neulet.2011.02.040 · DOI
  61. A Vezzani, 2011, The role of inflammation in epilepsy, Nat Rev Neurol, 7, 31, 10.1038/nrneurol.2010.178 · DOI · Paper page
  62. Y Gnatek, 2012, Acetylcholinesterase loosens the brain's cholinergic anti-inflammatory response and promotes epileptogenesis, Front Mol Neurosci, 5, 66, 10.3389/fnmol.2012.00066 · DOI
  63. T Ravizza, 2008, Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy, Neurobiology of Disease, 29, 142, 10.1016/j.nbd.2007.08.012 · DOI
  64. LA Shapiro, 2008, Rapid astrocyte and microglial activation following pilocarpine-induced seizures in rats, Epilepsia, 49, 33, 10.1111/j.1528-1167.2008.01491.x · DOI · Paper page
  65. E Avignone, 2008, Status Epilepticus Induces a Particular Microglial Activation State Characterized by Enhanced Purinergic Signaling, The Journal of Neuroscience, 28, 9133, 10.1523/JNEUROSCI.1820-08.2008 · DOI
  66. L Ulmann, 2013, Involvement of P2X4 receptors in hippocampal microglial activation after status epilepticus, Glia, 61, 1306, 10.1002/glia.22516 · DOI
  67. T Ravizza, 2006, Status epilepticus induces time-dependent neuronal and astrocytic expression of interleukin-1 receptor type I in the rat limbic system, NSC, 137, 301
  68. ML Foresti, 2009, Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine-induced status epilepticus, Journal of Neuroinflammation, 6, 40, 10.1186/1742-2094-6-40 · DOI
  69. J Abraham, 2012, Neurobiology of Disease, Neurobiology of Disease, 46, 425
  70. N Wang, 2015, Minocycline inhibits brain inflammation and attenuates spontaneous recurrent seizures following pilocarpine-induced status epilepticus, Neuroscience, 287, 144, 10.1016/j.neuroscience.2014.12.021 · DOI
  71. SX Jiang, 2012, Vimentin participates in microglia activation and neurotoxicity in cerebral ischemia, Journal of Neurochemistry, 122, 764, 10.1111/j.1471-4159.2012.07823.x · DOI
  72. GP Brennan, 2017, microRNAs in the pathophysiology of epilepsy, Neuroscience Letters
  73. JA Gorter, 2014, Hippocampal subregion-specific microRNA expression during epileptogenesis in experimental temporal lobe epilepsy, Neurobiology of Disease, 62, 508, 10.1016/j.nbd.2013.10.026 · DOI · Paper page
  74. NB Caberoy, 2012, Tubby regulates microglial phagocytosis through MerTK, Journal of Neuroimmunology, 252, 40, 10.1016/j.jneuroim.2012.07.009 · DOI
  75. SK Wyatt, 2017, Enhanced classical complement pathway activation and altered phagocytosis signaling molecules in human epilepsy, Experimental Neurology, 295, 184, 10.1016/j.expneurol.2017.06.009 · DOI
  76. R Raoof, 2017, Cerebrospinal fluid microRNAs are potential biomarkers of temporal lobe epilepsy and status epilepticus, Sci Rep, 7, 3328, 10.1038/s41598-017-02969-6 · DOI · Paper page
  77. SM Eacker, 2011, Neuronal activity regulates hippocampal miRNA expression, PLoS One, 6, e25068, 10.1371/journal.pone.0025068 · DOI
  78. Y Shinohara, 2011, miRNA profiling of bilateral rat hippocampal CA3 by deep sequencing, Biochemical and Biophysical Research Communications, 409, 293, 10.1016/j.bbrc.2011.05.004 · DOI
  79. JD Lambeth, 2004, NOX enzymes and the biology of reactive oxygen, Nat Rev Immunol, 4, 181, 10.1038/nri1312 · DOI · Paper page
  80. S-H Choi, 2012, Inhibition of NADPH oxidase promotes alternative and anti-inflammatory microglial activation during neuroinflammation, Journal of Neurochemistry, 120, 292, 10.1111/j.1471-4159.2011.07572.x · DOI
  81. MT Fischer, 2012, NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury, Brain, 135, 886, 10.1093/brain/aws012 · DOI · Paper page
  82. A Guemez-Gamboa, 2011, Activation of NOX2 by the stimulation of ionotropic and metabotropic glutamate receptors contributes to glutamate neurotoxicity in vivo through the production of reactive oxygen species and calpain activation, Journal of Neuropathology and Experimental Neurology, 70, 1020, 10.1097/NEN.0b013e3182358e4e · DOI
  83. Y Huo, 2011, Dexamethasone inhibits the Nox-dependent ROS production via suppression of MKP-1-dependent MAPK pathways in activated microglia, BMC Neurosci, 12, 49, 10.1186/1471-2202-12-49 · DOI
  84. Q Li, 2011, Alsin and SOD1(G93A) proteins regulate endosomal reactive oxygen species production by glial cells and proinflammatory pathways responsible for neurotoxicity, Journal of Biological Chemistry, 286, 40151, 10.1074/jbc.M111.279711 · DOI
  85. L Qin, 2012, NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration, Journal of Neuroinflammation, 9, 5, 10.1186/1742-2094-9-5 · DOI · Paper page
  86. B Hernández-Enríquez, 2011, Reactive oxygen species are related to ionic fluxes and volume decrease in apoptotic cerebellar granule neurons: role of NOX enzymes, Journal of Neurochemistry, 117, 654
  87. Y Ramiro-Cortés, 2011, Reactive oxygen species participate in the p38-mediated apoptosis induced by potassium deprivation and staurosporine in cerebellar granule neurons, International Journal of Biochemistry & Cell Biology, 43, 1373, 10.1016/j.biocel.2011.06.001 · DOI
  88. N Demaurex, 2009, 12, 819
  89. R Di Maio, 2011, Pilocapine alters NMDA receptor expression and function in hippocampal neurons: NADPH oxidase and ERK1/2 mechanisms, Neurobiology of Disease, 42, 482, 10.1016/j.nbd.2011.02.012 · DOI
  90. R Di Maio, 2013, Thiol oxidation and altered NR2B/NMDA receptor functions in in vitro and in vivo pilocarpine models: implications for epileptogenesis, Neurobiology of Disease, 49, 87, 10.1016/j.nbd.2012.07.013 · DOI
  91. RRF Pestana, 2010, Reactive oxygen species generated by NADPH oxidase are involved in neurodegeneration in the pilocarpine model of temporal lobe epilepsy, Neuroscience Letters, 484, 187, 10.1016/j.neulet.2010.08.049 · DOI
  92. JH Kim, 2013, Post-treatment of an NADPH oxidase inhibitor prevents, Brain Research, 1
  93. JS Ha, 2010, Extracellular hydrogen peroxide contributes to oxidative glutamate toxicity, Brain Research, 1359, 291, 10.1016/j.brainres.2010.08.086 · DOI
  94. EL Mead, 2012, Microglial neurotransmitter receptors trigger superoxide production in microglia; consequences for microglial-neuronal interactions, Journal of Neurochemistry, 121, 287, 10.1111/j.1471-4159.2012.07659.x · DOI
  95. M Patel, 2005, Activation of NADPH oxidase and extracellular superoxide production in seizure-induced hippocampal damage, Journal of Neurochemistry, 92, 123, 10.1111/j.1471-4159.2004.02838.x · DOI
  96. S Williams, 2015, Status epilepticus results in persistent overproduction of reactive oxygen species, inhibition of which is neuroprotective, Neuroscience, 303, 160, 10.1016/j.neuroscience.2015.07.005 · DOI
  97. A Pecorelli, 2015, NADPH oxidase activation and 4-hydroxy-2-nonenal/aquaporin-4 adducts as possible new players in oxidative neuronal damage presents in drug-resistant epilepsy, Biochim Biophys Acta, 1852, 507, 10.1016/j.bbadis.2014.11.016 · DOI
  98. S Tétrault, 2008, Opening of the blood-brain barrier during isoflurane anaesthesia, Eur J Neurosci, 28, 1330, 10.1111/j.1460-9568.2008.06443.x · DOI
  99. G Bar-Klein, 2016, Isoflurane prevents acquired epilepsy in rat models of temporal lobe epilepsy, Ann Neurol, 80, 896, 10.1002/ana.24804 · DOI
  100. D Sanoudou, 2006, Skeletal muscle repair in a mouse model of nemaline myopathy, Human Molecular Genetics, 15, 2603, 10.1093/hmg/ddl186 · DOI
  101. VG Tusher, 2001, Significance analysis of microarrays applied to the ionizing radiation response, Proc Natl Acad Sci USA, 98, 5116, 10.1073/pnas.091062498 · DOI · Paper page
  102. D Sanoudou, 2010, Role of Esrrg in the fibrate-mediated regulation of lipid metabolism genes in human ApoA-I transgenic mice, Pharmacogenomics J, 10, 165, 10.1038/tpj.2009.51 · DOI
  103. A Kel, 2006, Beyond microarrays: find key transcription factors controlling signal transduction pathways, BMC Bioinformatics, 7, S13, 10.1186/1471-2105-7-S2-S13 · DOI
  104. J Koschmann, 2015, “Upstream Analysis”: An Integrated Promoter-Pathway Analysis Approach to Causal Interpretation of Microarray Data, Microarrays (Basel), 4, 270, 10.3390/microarrays4020270 · DOI

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Authors
Kalozoumi, G., Kel-Margoulis, O., Vafiadaki, E., Greenberg, D., Bernard, H., Soreq, H., Depaulis, A., & Sanoudou, D.
Venue
PLOS ONE
Published
2018-08-16
Volume
13
Issue
8
Pages
e0201742
ISSN
1932-6203
Cited by
38
References
3
Language
en
Funders
  • INSERM
  • European Union 6th Framework Program for Research and Technological Development (VALAPODYN, contract # LSHG-CT-2006-037277)

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Kalozoumi, G., Kel-Margoulis, O., Vafiadaki, E., Greenberg, D., Bernard, H., Soreq, H., Depaulis, A., & Sanoudou, D. (2018). Glial responses during epileptogenesis in Mus musculus point to potential therapeutic targets. PLOS ONE. https://doi.org/10.1371/journal.pone.0201742