[The low expression of long non-coding RNA Linc00638 contributes to rheumatoid arthritis progression by regulating...

To investigate the expression of long non-coding RNA (lncRNA) Linc00638 in rheumatoid arthritis (RA) and its regulatory role in inflammation and oxidative stress of synovial fibroblasts in RA patients (RA-FLS).

Peripheral blood mononuclear cells (PBMCs) were collected from 20 healthy individuals and 35 RA patients for detecting the expression of Linc00638 using RT-qPCR to analyze the correlation of Linc00638 expression with the clinical indicators of RA patients. A Linc00638 overexpression plasmid and siRNA targeting Linc00638 were transfected into RA-FLS, and the changes in cell viability was observed using CCK8 assay; the changes in the expression levels of interleukin-4 (IL-4), IL-6, reactive oxygen species (ROS) and superoxide dismutase (SOD) in the supernatant were detected using ELISA.

Compared with the healthy control subjects, RA patients had significantly increased ESR, CRP, RF, anti-CCP, IgA, and C4 levels (P < 0.05) and significantly decreased Linc00638 expression in the PBMCs (P < 0.01). The area under the receiver-operating characteristic (ROC) curve of Linc00638 was 91.86% with the best cut-off value of 0.74 for diagnosis of RA. Spearman correlation analysis showed that Linc00638 expression level was negatively correlated with age, course of disease, DAS28, ESR, CRP, RF and anti-CCP, and positively correlated with IL-4 and SOD levels (P < 0.05). Association rule analysis showed that a decreased Linc00638 expression was strongly correlated with an increase of age (>60 years), a longer disease course (>10 years), elevated levels of ESR, RF and anti-CCP, and decreased levels of IL-4 and SOD. In RA-FLS, overexpression of Linc00638 significantly inhibited while Linc00638 interference obviously enhanced the cell viability. Over-expression of Linc00638 also significantly increased the levels of IL-4 and SOD (P < 0.05) and decreased the expressions of IL-6 and ROS (P < 0.05), while interference of Linc00638 produced the opposite effects in the cells (P < 0.05).

RA patients have low expression levels of Linc00638, which may participate in disease progression by regulating inflammation and oxidative stress.