Abstract
The expression of selected microRNAs (miRNAs) known to be involved in the regulation of immune responses was analyzed in 74 patients with relapsing remitting multiple sclerosis (RRMS) and 32 healthy controls. Four miRNAs (miR-326, miR-155, miR-146a, miR-142-3p) were aberrantly expressed in peripheral blood mononuclear cells from RRMS patients compared to controls. Although expression of these selected miRNAs did not differ between treatment-naïve (n = 36) and interferon-beta treated RRMS patients (n = 18), expression of miR-146a and miR-142-3p was significantly lower in glatiramer acetate (GA) treated RRMS patients (n = 20) suggesting that GA, at least in part, restores the expression of deregulated miRNAs in MS.
Highlights
MicroRNAs have recently emerged as potential biomarkers of disease in different autoimmune disorders including rheumatoid arthritis [1], systemic lupus erythematosus [2] or Sjogren’s syndrome [3]. miRNAs are short (,22 nucleotides) noncoding RNA molecules that regulate gene expression at the posttranscriptional level
Recent data indicate that miRNA dysregulation may contribute to the pathogenesis of multiple sclerosis (MS): Overexpression of miRNAs that target CD47 was found to contribute to macrophage-mediated damage in active MS lesions and miRNA expression profiling in whole blood or leukocytes derived from MS patients suggests an aberrant expression of various miRNAs in the peripheral immune compartment [6,7]
We studied the expression of five selected miRNA in peripheral blood mononuclear cells (PBMC) derived from treatment naıve patients with relapsing-remitting multiple sclerosis (RRMS) (n = 36) and healthy controls (HC, n = 32)
Summary
MicroRNAs (miRNAs) have recently emerged as potential biomarkers of disease in different autoimmune disorders including rheumatoid arthritis [1], systemic lupus erythematosus [2] or Sjogren’s syndrome [3]. miRNAs are short (,22 nucleotides) noncoding RNA molecules that regulate gene expression at the posttranscriptional level. One miRNA may target several hundreds of messenger RNAs and it has been proposed that up to 50% of mammalian genes underlay miRNA fine-tuning [4]. Recent data indicate that miRNA dysregulation may contribute to the pathogenesis of multiple sclerosis (MS): Overexpression of miRNAs that target CD47 was found to contribute to macrophage-mediated damage in active MS lesions and miRNA expression profiling in whole blood or leukocytes derived from MS patients suggests an aberrant expression of various miRNAs in the peripheral immune compartment [6,7]. We studied the expression of five selected immunologically relevant miRNAs in peripheral blood mononuclear cells (PBMC) derived from patients with relapsing-remitting multiple sclerosis (RRMS) and healthy controls and addressed the impact of immunomodulatory therapy on miRNA expression by comparing treatment-naıve to glatiramer acetate (GA) or interferon-beta (IFN-beta) treated patients
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