Plasma expression and bioinformatic analysis of Mir-16, Mir-132, Mir-146 and Mir-223 in patients with rheumatoid arthritis

Abstract

Background

MicroRNAs (miRNAs) are involved in the pathogenesis of rheumatoid arthritis (RA) through modulating gene expression.

Aim

To assess the plasma expression of miR-16, miR-132, miR-146 and miR-223 in patients with RA and their relation to activity and severity of the disease and their potential value as biomarkers. Through bioinformatics study we aimed to determine the predictor target genes of the studied miRNAs to clarify their role in RA pathogenesis.

Methods

The study comprised 73 patients suffering from RA and 50 healthy individuals. We used the disease activity score-28 (DAS-28) to assess disease activity. Joint damage was assessed by Kaarela and Kautiainen modification of Larsen scale. Anti-anticyclic citrullinated peptide (anti-CCP) antibodies, serum high sensitive C reactive protein (hsCRP) and rheumatoid factor (RF) were assayed by ELISA. Plasma miR-223, miR-146a, miR-16 and miR-132 were quantified by qRT-PCR followed by a simple dry laboratory analysis of the involved target genes of the studied miRNAs in RA pathogenesis by KEGG pathways.

Results

In comparison to controls, RA patients showed overexpressed miR-146a, miR-223and miR-16, while miR-132 was down-regulated. Additionally, miR-146a correlated positively with DAS28, anti-CCP antibodies and RF. Bioinformatics revealed that the predicted targeted genes of miR-146a, miR-16, miR-223 and miR-132 are potential contributing factors for RA pathogenesis and bone degradation.

Conclusion

miR-146a, miR-223, miR-16 and miR-132 may be potential non-invasive molecular biomarkers for RA diagnosis. Plasma miR-146a might be considered as potential biomarker for disease activity. The predicted genes targeted by miR-146a, miR-223, miR-16 and miR-132 are implicated in RA pathogenesis and ultimately can be used in future target therapeutic approach.