4.5 Article

Pro-Inflammatory Cytokines and Antibodies Induce hnRNP A1 Dysfunction in Mouse Primary Cortical Neurons

Journal

BRAIN SCIENCES
Volume 11, Issue 10, Pages -

Publisher

MDPI
DOI: 10.3390/brainsci11101282

Keywords

RNA-binding protein; multiple sclerosis; stress granules; heterogeneous nuclear ribonucleoprotein A1; cytokines; autoimmunity

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Funding

  1. Department of Medicine at the University of Saskatchewan
  2. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair at the University of Saskatchewan

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The study demonstrates that primary neurons exposed to pro-inflammatory cytokines and anti-A1 antibodies, characteristic of an MS autoimmune response, exhibit increased A1 mislocalization, stress granule formation, and decreased neurite length, indicating a significant relationship between secreted immune factors, A1 dysfunction, and neuronal damage in a disease-relevant model system.
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system with a significant neurodegenerative component. Dysfunctional RNA-binding proteins (RBPs) are causally linked to neuronal damage and are a feature of MS, including the mislocalization of the RBP heterogeneous nuclear ribonucleoprotein A1 (A1). Here, we show that primary neurons exposed to pro-inflammatory cytokines and anti-A1 antibodies, both characteristic of an MS autoimmune response, displayed increased A1 mislocalization, stress granule formation, and decreased neurite length, a marker of neurodegeneration. These findings illustrate a significant relationship between secreted immune factors, A1 dysfunction, and neuronal damage in a disease-relevant model system.

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