[miR-185-5p alleviates the inflammatory response of acute gouty arthritis by inhibiting of IL-1β].

Objective To investigate the relationship between interleukin-1β (IL-1β) and miR-185-5p in the process of joint injury in acute gouty arthritis (AGA). Methods The serum miR-185-5p levels of 89 AGA patients and 91 healthy volunteers were detected by real-time quantitative PCR. The correlation between miR-185-5p expression level and VAS score or IL-1β expression level was evaluated by Pearson correlation coefficient method.

Downregulation of microRNA-101-3p participates in systemic lupus erythematosus progression via negatively regulating HDAC9.

This study aimed to investigate the mechanism of microRNA-101-3p (miR-101-3p) on the progression of systemic lupus erythematosus (SLE). The human peripheral blood mononuclear cells (PBMCs) were isolated from whole blood samples of SLE patients and healthy individuals, followed by cell culture and transfection. Moreover, the flow cytometry assay, quantitative real-time reverse-transcription polymerase chain reaction, Western blot, and enzyme-linked immunoassay were used to assess the effect of miR-101-3p on PBMCs.

Long noncoding RNA profiling revealed differentially expressed lncRNAs associated with disease activity in PBMCs from patients with rheumatoid arthritis.

Long noncoding RNAs (lncRNAs) have recently emerged as important biological regulators, and the aberrant expression of lncRNAs has been reported in numerous diseases. However, the expression of lncRNAs in peripheral blood mononuclear cells (PBMCs) in rheumatoid arthritis (RA) has not been well documented. We applied a microarray analysis to profile the lncRNA and mRNA expression in 3 pairs of samples.

Elevated expression of microRNA-873 facilitates Th17 differentiation by targeting forkhead box O1 (Foxo1) in the pathogenesis of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, and its pathogenesis remains mostly unknown. MicroRNAs (miRs) has drawn much attention as a crucial regulator of autoimmune diseases. In this study, we demonstrated that miR-873 expression was significantly up-regulated in patients with SLE, and its expression was positively associated with the disease severity.