Abstract
MiR-150 regulates maturation and differentiation of T cells but how it functions in multiple sclerosis (MS) is unclear. In miR-150 knockout (KO) mice, we examined the effect of miR-150 deletion on disease severity of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. After deleting miR-150, EAE disease severity was reduced according to clinical score. Histological staining and MBP immunofluorescence staining revealed that miR-150 deletion limited the extent of inflammatory demyelination and axonal damage in the spinal cord. Flow cytometry showed that CD3+, CD4+, and CD8+ T cells were increased in WT-EAE mice, but miR-150 deletion significantly reversed EAE-mediated up-regulation of CD3+, CD4+, and CD8+ T cells and down-regulation of CD19+ B cells. In addition, miR-150 deletion reduced the mRNA expression of IL-1β, IL-6, IL-17, and TNF-α in spleen and spinal cord after EAE induction. Thus, miR-150 deletion reduces EAE severity and demyelination, probably through inhibiting the activated immune response and the inflammation in the central nervous system.
Highlights
MicroRNAs are a class of short (20–25 nucleotides) single stranded molecules that regulate gene expression at the post-transcriptional level
We observed that EAE challenge induced Myelin Basic Protein (MBP) loss in wild type (WT)-EAE group compared with WT group, whereas miR-150 KO resulted in a significant increase in MBP expression in KO-EAE group compared with WT-EAE group (Figure 2D)
These results suggest that deletion of miR-150 reduces myelin pathology after EAE challenge
Summary
MicroRNAs (miRNAs) are a class of short (20–25 nucleotides) single stranded molecules that regulate gene expression at the post-transcriptional level. Single stranded RNA molecules bind to an RNA-inducing silencing complex to form a miRNA/RISC-complex which can interact with target mRNA and effect mRNA degradation or the inhibition of protein translation. This leads to reduction of target protein synthesis (Carissimi et al, 2009). Among miRNAs involved in the immune response, miR-150 is noted for selective expression in immature, resting B and T cells (Monticelli et al, 2005a)
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