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01-10-2019 | Multiple Sclerosis | Original Article

Down-regulation of ERMN expression in relapsing remitting multiple sclerosis

Authors: Behnaz Salek Esfahani, Jalal Gharesouran, Soudeh Ghafouri-Fard, Shahrzad Talebian, Shahram Arsang-Jang, Mir Davood Omrani, Mohammad Taheri, Maryam Rezazadeh

Published in: Metabolic Brain Disease | Issue 5/2019

Abstract

Multiple Sclerosis (MS) is a chronic inflammatory disease causing demyelination and neurodegeneration in the central nervous system (CNS). Although the exact etiology of MS is still unclear, both genetic and environmental elements are regarded as causative factors. Environmental factors can induce a cascade of events in immune system leading to neuronal death and nerve demyelination. This paper aims to compare the peripheral transcript levels of Ermin (ERMN) (a gene with putative role in cytoskeletal rearrangements during myelinogenesis) and Listerin E3 Ubiquitin Protein Ligase 1 (LTN1) (a gene with functions in regulating innate immune system) between relapsing-remitting MS (RR-MS) patients and healthy controls. The results showed a significant decrease in ERMN expression (p = 0.022); whereas, no significant difference was detected in LTN1 expression between two groups (p = 0.935). The reduction in ERMN expression in leukocytes could be the cause of demyelinating process in RR-MS patients. Current findings might also have practical importance in prognosis and targeted therapies.

Baecher-Allan C, Kaskow BJ, Weiner HL (2018) Multiple sclerosis: mechanisms and immunotherapy. Neuron 97:742–768CrossRefPubMed

Bengtson MH, Joazeiro CAP (2010) Role of a ribosome-associated E3 ubiquitin ligase in protein quality control. Nature 467:470–473CrossRefPubMedPubMedCentral

Brockschnieder D, Sabanay H, Riethmacher D, Peles E (2006) Ermin, a myelinating oligodendrocyte-specific protein that regulates cell morphology. J Neurosci 26:757–762CrossRefPubMedPubMedCentral

Choe Y-J, Park S-H, Hassemer T, Körner R, Vincenz-Donnelly L, Hayer-Hartl M, Hartl FU (2016) Failure of RQC machinery causes protein aggregation and proteotoxic stress. Nature 531:191–195CrossRefPubMed

Chu J, Hong NA, Masuda CA, Jenkins BV, Nelms KA, Goodnow CC, Glynne RJ, Wu H, Masliah E, Joazeiro CAP, Kay SA (2009) A mouse forward genetics screen identifies LISTERIN as an E3 ubiquitin ligase involved in neurodegeneration. Proc Natl Acad Sci 106:2097–2103CrossRefPubMedPubMedCentral

Defenouillère Q, Zhang E, Namane A, Mouaikel J, Jacquier A, Fromont-Racine M (2016) Rqc1 and Ltn1 prevent C-terminal Alanine-Threonine Tail (CAT-tail)-induced protein aggregation by efficient recruitment of Cdc48 on stalled 60S subunits. J Biol Chem 291:12245–12253CrossRefPubMedPubMedCentral

Dendrou CA, Fugger L, Friese MA (2015) Immunopathology of multiple sclerosis. Nat Rev Immunol 15:545–558CrossRefPubMed

Di Filippo M, Portaccio E, Mancini A, Calabresi P (2018) Multiple scle- rosis and cognition: synaptic failure and network dysfunction. Nat Rev Neurosci. 19(10):599-609. https://doi.org/10.1038/s41583-018-0053-9.

Eskandarieh S, Heydarpour P, Minagar A, Pourmand S, Sahraian MA (2016) Multiple sclerosis epidemiology in East Asia, south East Asia and South Asia: a systematic review. Neuroepidemiology 46:209–221CrossRefPubMed

Friese MA, Schattling B, Fugger L (2014) Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. Nat Rev Neurol 10:225CrossRefPubMed

Homs A, Codina-Solà M, Rodríguez-Santiago B, Villanueva C, Monk D, Cuscó I, Pérez-Jurado L (2016) Genetic and epigenetic methylation defects and implication of the ERMN gene in autism spectrum disorders. Transl Psychiatry 6:e855CrossRefPubMedPubMedCentral

Huang WJ, Chen WW, Zhang X (2017) Multiple sclerosis: pathology, diagnosis and treatments. Exp Ther Med 13:3163–3166CrossRefPubMedPubMedCentral

Lassmann H, van Horssen J (2011) The molecular basis of neurodegeneration in multiple sclerosis. FEBS Lett 585:3715–3723CrossRefPubMed

Lehmann ML, Weigel TK, Elkahloun AG, Herkenham M (2017) Chronic social defeat reduces myelination in the mouse medial prefrontal cortex. Sci Rep 7:46548CrossRefPubMedPubMedCentral

Martins-de-Souza D, Gattaz WF, Schmitt A, Rewerts C, Maccarrone G, Dias-Neto E, Turck CW (2009a) Prefrontal cortex shotgun proteome analysis reveals altered calcium homeostasis and immune system imbalance in schizophrenia. Eur Arch Psychiatry Clin Neurosci 259:151–163CrossRefPubMed

Martins-de-Souza D, Gattaz WF, Schmitt A, Rewerts C, Marangoni S, Novello JC, Maccarrone G, Turck CW, Dias-Neto E (2009b) Alterations in oligodendrocyte proteins, calcium homeostasis and new potential markers in schizophrenia anterior temporal lobe are revealed by shotgun proteome analysis. J Neural Transm 116:275–289CrossRefPubMed

Mazdeh M, Taheri M, Sayad A, Bahram S, Omrani MD, Movafagh A, Inoko H, Akbari MT, Noroozi R, Hajilooi M (2016) HLA genes as modifiers of response to IFN-β-1a therapy in relapsing-remitting multiple sclerosis. Pharmacogenomics 17:489–498CrossRefPubMed

Pérez-Cerdá F, Sánchez-Gómez MV, Matute C (2016) The link of inflammation and neurodegeneration in progressive multiple sclerosis. Mult Scler Demyelinating Disord 1:9CrossRef

Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, Fujihara K, Havrdova E, Hutchinson M, Kappos L, Lublin FD, Montalban X, O'connor P, Sandberg-Wollheim M, Thompson AJ, Waubant E, Weinshenker B, Wolinsky JS (2011) Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 69:292–302CrossRefPubMedPubMedCentral

Rahimi M, Aghabozorg Afjeh SS, Omrani MD, Arsang-Jang S, Ganji M, Noroozi R, Taheri M, Ghafouri-Fard S (2018) Soluble Receptor for Advanced Glycation End Products (sRAGE) is Up-Regulated in multiple sclerosis patients treated with Interferon beta-1a. Cell Physiol Biochem 46:561–567CrossRefPubMed

Sawcer S, Franklin RJM, Ban M (2014) Multiple sclerosis genetics. Lancet Neurol 13:700–709CrossRefPubMed

Sayad A, Ghafouri-Fard S, Omrani MD, Noroozi R, Taheri M (2017) Myxovirus resistance protein A (MxA) polymorphism is associated with IFNbeta response in Iranian multiple sclerosis patients. Neurol Sci 38:1093–1099CrossRefPubMed

Tyburczy ME, Kotulska K, Pokarowski P, Mieczkowski J, Kucharska J, Grajkowska W, Roszkowski M, Jozwiak S, Kaminska B (2010) Novel proteins regulated by mTOR in subependymal giant cell astrocytomas of patients with tuberous sclerosis complex and new therapeutic implications. Am J Pathol 176:1878–1890CrossRefPubMedPubMedCentral

Wang T, Jia L, Lv B, Liu B, Wang W, Wang F, Yang G, Bu X, Yao L, Zhang B (2011) Human Ermin (hErmin), a new oligodendrocyte-specific cytoskeletal protein related to epileptic seizure. Brain Res 1367:77–84CrossRefPubMed

Wang F, Canadeo LA, Huibregtse JM (2015) Ubiquitination of newly synthesized proteins at the ribosome. Biochimie 114:127–133CrossRefPubMedPubMedCentral

Xu H (2014) Neurodegenerative mechanisms of multiple sclerosis. JSM Neurosurg Spine 2:1024

Title: Down-regulation of ERMN expression in relapsing remitting multiple sclerosis
Authors: Behnaz Salek Esfahani
Jalal Gharesouran
Soudeh Ghafouri-Fard
Shahrzad Talebian
Shahram Arsang-Jang
Mir Davood Omrani
Mohammad Taheri
Maryam Rezazadeh
Publication date: 01-10-2019
Publisher: Springer US
Keyword: Multiple Sclerosis
Published in: Metabolic Brain Disease / Issue 5/2019
Print ISSN: 0885-7490
Electronic ISSN: 1573-7365
DOI: https://doi.org/10.1007/s11011-019-00429-w

2024 ASCO Annual Meeting

Springer Medicine

Down-regulation of ERMN expression in relapsing remitting multiple sclerosis

Abstract

2024 ASCO Annual Meeting

Springer Medicine

Abstract

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