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Increased Post-Translational Lysine Acetylation of Myelin Basic Protein Is Associated with Peak Neurological Disability in a Mouse Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis
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    Increased Post-Translational Lysine Acetylation of Myelin Basic Protein Is Associated with Peak Neurological Disability in a Mouse Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis
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    The Rady Faculty of Health Sciences, College of Pharmacy, Pharmaceutical Analysis Laboratory, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada
    The Rady Faculty of Health Sciences, College of Pharmacy, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada
    § Department of Human Anatomy and Cell Science, College of Medicine, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada
    Joint Laboratory of Biological Psychiatry Between Shantou University Medical College and College of Medicine, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada
    Department of Rehabilitation Medicine, Health Sciences Centre (HSC), Winnipeg, Manitoba R3A 1R9, Canada
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    Journal of Proteome Research

    Cite this: J. Proteome Res. 2018, 17, 1, 55–62
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    https://doi.org/10.1021/acs.jproteome.7b00270
    Published November 7, 2017
    Copyright © 2017 American Chemical Society

    Abstract

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    Citrullination of arginine residues is a post-translational modification (PTM) found on myelin basic protein (MBP), which neutralizes MBPs positive charge, and is implicated in myelin damage and multiple sclerosis (MS). Here we identify lysine acetylation as another neutralizing PTM to MBP that may be involved in myelin damage. We quantify changes in lysine and arginine PTMs on MBP derived from mice induced with an experimental autoimmune encephalomyelitis (EAE) model of MS using liquid chromatography tandem mass spectrometry. The changes in PTMs are correlated to changes in neurological disability scoring (NDS), as a marker of myelin damage. We found that lysine acetylation increased by 2-fold on MBP during peak NDS post-EAE induction. We also found that mono- and dimethyl-lysine, as well as asymmetric dimethyl-arginine residues on MBP were elevated at peak EAE disability. These findings suggest that the acetylation and methylation of lysine on MBP are PTMs associated with the neurological disability produced by EAE. Since histone deacetylase (HDAC) inhibitors have been previously shown to improve neurological disability, we also show that treatment with trichostatin A (a HDAC inhibitor) improves the NDS of EAE mice but does not change MBP acetylation.

    Copyright © 2017 American Chemical Society

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    This article is cited by 12 publications.

    1. Kumar D. Shanmukha, Harikrishnareddy Paluvai, Santosh K. Lomada, Mahesh Gokara, Suresh K. Kalangi. Histone deacetylase (HDACs) inhibitors: Clinical applications. 2023, 119-152. https://doi.org/10.1016/bs.pmbts.2023.02.011
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    4. Licia C. Silva-Costa, Bradley J. Smith. Post-translational Modifications in Brain Diseases: A Future for Biomarkers. 2022, 129-141. https://doi.org/10.1007/978-3-031-05460-0_10
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    8. Surabhi Shukla, Babu L. Tekwani. Histone Deacetylases Inhibitors in Neurodegenerative Diseases, Neuroprotection and Neuronal Differentiation. Frontiers in Pharmacology 2020, 11 https://doi.org/10.3389/fphar.2020.00537
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    10. Vaibhav Singh, Ajai Tripathi, Ranjan Dutta. Proteomic Approaches to Decipher Mechanisms Underlying Pathogenesis in Multiple Sclerosis Patients. PROTEOMICS 2019, 19 (16) https://doi.org/10.1002/pmic.201800335
    11. Lei Sun, Elphine Telles, Molly Karl, Fengdong Cheng, Noreen Luetteke, Eduardo M Sotomayor, Robert H Miller, Edward Seto. Loss of HDAC11 ameliorates clinical symptoms in a multiple sclerosis mouse model. Life Science Alliance 2018, 1 (5) , e201800039. https://doi.org/10.26508/lsa.201800039
    12. Hao Qiu, Yanzhi Guo, Lezheng Yu, Xuemei Pu, Menglong Li. Predicting protein lysine methylation sites by incorporating single-residue structural features into Chou's pseudo components. Chemometrics and Intelligent Laboratory Systems 2018, 179 , 31-38. https://doi.org/10.1016/j.chemolab.2018.05.007

    Journal of Proteome Research

    Cite this: J. Proteome Res. 2018, 17, 1, 55–62
    Click to copy citationCitation copied!
    https://doi.org/10.1021/acs.jproteome.7b00270
    Published November 7, 2017
    Copyright © 2017 American Chemical Society

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