Objective To investigate the expression and clinical significance of long non‐coding RNA taurine up‐regulated gene 1 (lncRNA TUG1) in the peripheral blood of systemic lupus erythematosus (SLE) patients. Methods With the peripheral blood mononuclear cells (PBMCs: T‐cells, B‐cells and monocytes) collected from SLE patients and healthy controls, TUG1 expression was determined to identify the correlation with the clinicopathological features of SLE patients. Thereby, the diagnostic value of TUG1 expression in diagnosis of SLE was evaluated by receiver operating characteristic (ROC) curve analysis. Results As compared to healthy controls, SLE patients manifested a lower expression of TUG1 in PBMCs, which was further decreased in SLE patients with lupus nephritis (P < .05). The lowest level of TUG1 was found in monocytes, rather than T‐cells or B‐cells (P < .05). Negative correlations were identified between TUG1 levels and SLE Disease Activity Index score (r = −.904, P < .001), erythrocyte sedimentation rate (r = −.779, P < .001), disease duration (r = −.503, P < .001) and 24‐hour urinary protein (r = −.807, P < .001). Complement C3 levels were positively associated with TUG1 expression (r = .817, P < .001). In addition, the area under the ROC curve of diagnostic efficiency for SLE based on TUG1 was 0.982, and 0.930 for SLE with lupus nephritis. Conclusions The levels of lncRNA TUG1 was markedly lower in the SLE patients, which was more obvious in SLE patients with lupus nephritis, and thus, it could be a promising clinical diagnostic tool for SLE patients or SLE patients with lupus nephritis.

We aimed to know the effect of nuclear factor‐kappa B (NF‐κB) inhibition on the kidney injury of systemic lupus erythematosus (SLE) mice. Pristane‐induced SLE mice were treated with pyrrolidine dithiocarbamate (PDTC, 50 or 100 mg/kg), a NF‐κB inhibitor. Histopathological changes were observed by hematoxylin & eosin, Masson and periodic schiff‐methenamine stainings. Long noncoding RNA Taurine upregulated gene 1 (LncRNA TUG1) was measured by real‐time reverse transcription PCR, NF‐κB p65 expression by western blotting, levels of inflammatory cytokines, antinuclear antibodies (ANA), and antidouble stranded DNA (anti‐dsDNA) by enzyme‐linked immunosorbent assay, and the deposition of IgG and C3 by immunofluorescence. The kidney of SLE mice exhibited interstitial inflammatory cell infiltration, interstitial fibrous proliferation, glomerular mesangial proliferation, and crescent formation, which was mitigated after PDTC administration. The levels of BUN, Cr, ANA, and anti‐dsDNA and the pro‐inflammatory factors in SLE mice were increased with obvious deposition of IgG and C3, but they were also reversed by PDTC. Furthermore, the NF‐κB p65 expression in the nucleus in the SLE mice was decreased with the up‐regulation of TUG1 expression and NF‐κB p65 expression in the cytoplasm after PDTC treatment. Correlation analysis revealed the negative correlation between the TUG1 expression and NF‐κB p65 in the nucleus in the kidney tissues. NF‐κB inhibition with PDTC protected against the kidney injury of pristine‐induced SLE mice possibly via up‐regulating lncRNA TUG1, and further clinical studies are needed to clarify whether NF‐κB inhibition may be a therapeutic modality for the kidney injury of SLE.

Aim: The aim of this study was to find potential differentially expressed long noncoding RNAs (lncRNAs) and mRNAs in systemic lupus erythematosus. Materials & methods: Differentially expressed lncRNAs and mRNAs were obtained in the Gene Expression Omnibus dataset. Functional annotation of differentially expressed mRNAs was performed, followed by protein–protein interaction network analysis. Then, the interaction network of lncRNA-nearby targeted mRNA was built. Results: Several interaction pairs of lncRNA-nearby targeted mRNA including NRIR-RSAD2, RP11-153M7.5-TLR2, RP4-758J18.2-CCNL2, RP11-69E11.4-PABPC4 and RP11-496I9.1-IRF7/ HRAS/ PHRF1 were identified. Measles and MAPK were significantly enriched signaling pathways of differentially expressed mRNAs. Conclusion: Our study identified several differentially expressed lncRNAs and mRNAs. And their interactions may play a crucial role in the process of systemic lupus erythematosus.