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In silico Analysis of Transcriptomic Profiling and Affected Biological pathways in Multiple Sclerosis

View ORCID ProfileRutvi Vaja, View ORCID ProfileHarpreet Kaur, View ORCID ProfileMohit Mazumder, View ORCID ProfileElia Brodsky
doi: https://doi.org/10.1101/2021.08.15.456398
Rutvi Vaja
1School of Science, Navrachana University, Gujarat, India
2Pine Biotech, New Orleans, USA
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  • ORCID record for Rutvi Vaja
  • For correspondence: vajarutvi@gmail.com
Harpreet Kaur
2Pine Biotech, New Orleans, USA
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Mohit Mazumder
2Pine Biotech, New Orleans, USA
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Elia Brodsky
2Pine Biotech, New Orleans, USA
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Abstract

Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease that is widely associated with Grey and white matter degradation due to the demyelination of axons. Thus exposing the underlying causes of this condition can lead to a novel treatment approach for Multiple Sclerosis. The total RNA microarray processed data from GEO for Multiple sclerotic patients was comprehensively analyzed to find out underlying differences between Grey Matter lesions (GML), Normal appearing Grey Matter (NAGM), and Control Grey matter at the transcriptomics level. Thus, in the current study, we performed various bioinformatics analyses on transcriptional profiles of 184 samples including 105 NAGM, 37 GML, and 42 Controls obtained from the NCBI-Bio project (PRJNA543111). First, exploratory data analysis based on gene expression data using principal component analysis (PCA) depicted distinct patterns between GML and CG samples. Subsequently, the Welch’s T-test differential gene expression analysis identified 1525 significantly differentially expressed genes (p.adj value <0.05, Fold change(>=+/-1.5) between these conditions. This study reveals the genes like CREB3L2, KIF5B, WIPI1, EP300, NDUFA1, ATG101, AND TAF4 as the key features that may substantially contribute to loss of cognitive functions in Multiple sclerosis and several other neurodegenerative disorders. Further, this study also proposes genes associated with Huntington’s disease in Multiple sclerotic patients. Eventually, the results presented here reveal new insights into MS and how it affects the development of male primary sexual characteristics.

Competing Interest Statement

The authors have declared no competing interest.

Footnotes

  • Emails of Authors: Rutvi Vaja: vajarutvi{at}gmail.com; Harpreet Kaur: hks04180{at}gmail.com; harpreet{at}pine.bio; Elia Brodsky: elia{at}pine.bio; Mohit Mazumder: mohit{at}pine.bio;

  • Abbreviations

    MS
    Multiple Sclerosis
    GML
    Grey matter lesions
    CGM
    Control Grey matter
    CG
    Control Samples
    NAMG
    Normal appearing Grey Matter
    CNS
    Central nervous system
    HD
    Huntington’s Disease
    WIPI1
    WD Repeat Domain, Phosphoinositide Interacting 1
    CREB
    cAMP response element-binding protein
  • Copyright 
    The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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    Posted August 17, 2021.
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    In silico Analysis of Transcriptomic Profiling and Affected Biological pathways in Multiple Sclerosis
    Rutvi Vaja, Harpreet Kaur, Mohit Mazumder, Elia Brodsky
    bioRxiv 2021.08.15.456398; doi: https://doi.org/10.1101/2021.08.15.456398
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    In silico Analysis of Transcriptomic Profiling and Affected Biological pathways in Multiple Sclerosis
    Rutvi Vaja, Harpreet Kaur, Mohit Mazumder, Elia Brodsky
    bioRxiv 2021.08.15.456398; doi: https://doi.org/10.1101/2021.08.15.456398

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