Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (7): 1471-1472.doi: 10.4103/1673-5374.330598

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Neuronal and endothelial transglutaminase-2 expression in experimental autoimmune encephalomyelitis and multiple sclerosis

Damien D. Pearse, Mousumi Ghosh*   

  1. Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA  (Pearse DD, Ghosh M) 
    Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA (Pearse DD, Ghosh M)
    Neuroscience Program, Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL, USA (Pearse DD)
    Department of Veterans Affairs, Veterans Affairs Medical Center, Miami, FL, USA (Pearse DD, Ghosh M)
  • Online:2022-07-15 Published:2022-01-15
  • Contact: Mousumi Ghosh, PhD, mghosh@med.miami.edu.
  • Supported by:
    This research was supported by The John M. and Jocelyn H.K. Watkins Distinguished Chair in Cell Therapies (to DDP) and The Miami Project to Cure Paralysis and The Buoniconti Fund (to DDP and MG).

Abstract: Multiple sclerosis (MS) is a neurological condition characterized by the disruption of the blood-brain barrier, immune system activation, and inflammation that is accompanied by glial reactivity, neuronal cell death, axon demyelination, and axotomy. Pathological changes result in functional loss including paralysis, migraine, vision problems, spasticity, and neuropathic pain. Although the causative factor responsible for triggering MS remains to be identified, anti-inflammatory treatments have been translated to clinical use with favorable reductions in the frequency, severity, and duration of relapses in the relapsing-remitting form of MS. Among the identified therapeutic targets in MS, transglutaminase-2 (TG2) has been reported to be involved in disease pathogenesis (Chrobok et al., 2018).