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
Categories
Funding
- Department of Medicine at the University of Saskatchewan
- Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair at the University of Saskatchewan
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available