CKS2 and S100A12: Two Novel Diagnostic Biomarkers for Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic systematicness autoimmunity disease with joint inflammation. RA etiology is still unknown. Early and exact diagnosing is still hard to reach. In the paper, we purposed to discover novel diagnosis biological marker for RA. Two open, usable gene expression profiles of human RA as well as controlled specimens (dataset GSE17755 as well as GSE93272) were downloaded from the GEO database. Differentially expressed genes (DEGs) were screened between 331 RA and 88 control samples. Functional enrichment analysis was applied to explore the possible function of DEGs. Expression levels as well as diagnosis values of biological marker in RA were further verified in our cohort by the use of RT-PCR and ROC assays. We identified 13 DEGs between RA samples and control samples. 13 DEGs were remarkably abundant in NF-kappa B signal pathway. Among the 13 DEGs, CKS2, S100A12, LY96, and ANXA3 exhibited a strong diagnostic ability in screening RA specimens from normal specimens using all AUC > 0.8. Moreover, we confirmed that the expression of CKS2 and S100A12 was distinctly upregulated in RA specimens contrasted to normal specimens. Overall, serum CKS2 and S100A12 could be used as novel diagnosis biological markers for RA patients.

Long non-coding RNA TSPEAR Antisense RNA 2 is downregulated in rheumatoid arthritis and inhibits the apoptosis of fibroblast-like synoviocytes by downregulating microRNA-212-3p (miR-212-3p).

Long non-coding RNA (lncRNA) TSPEAR-AS2 (TSPEAR Antisense RNA 2) participates in many human diseases, while its roles in rheumatoid arthritis (RA) are unknown. Plasma expression levels of TSPEAR-AS2 and microRNA (miR)-212-3p in both RA patients and healthy controls were measured by RT-qPCR. Diagnostic potentials of plasma TSPEAR-AS2 and miR-212-3p were assessed by ROC curve analysis. Normalized expression levels of TSPEAR-AS2 and miR-212-3p were subjected to Pearson's correlation coefficient to evaluate their corrections. TSPEAR-AS2 was significantly downregulated in RA patients, while plasma expression levels of miR-212-3p were significantly increased in RA patients. The expression of TSPEAR-AS2 and miR-212-3p showed promising diagnostic value for RA. Plasma expression levels of TSPEAR-AS2 and miR-212-3p were significantly and inversely correlated in RA patients but not in healthy controls. Besides, overexpression of TSPEAR-AS2 decreased the apoptosis of RA HFLSs, while miR-212-3p increased cell apoptosis. In addition, miR-212-3p attenuated the effects of overexpression of TSPEAR-AS2. Overexpression of TSPEAR-AS2 decreased the expression levels of miR-212-3p in HFLS, while overexpression of miR-212-3p did not affect the expression of TSPEAR-AS2. In conclusion, TSPEAR-AS2 is downregulated in RA and its overexpression can decrease the apoptosis of RA HFLSs by downregulating miR-212-3p.

[Oxidation status and γ-glutamylcysteine synthetase expression in the kidney of MRL/lpr lupus mice].

OBJECTIVE: [corrected] To investigate the role of glutathione (GSH) and γ-glutamylcysteine synthetase (γ-GCS) in lupus nephritis. METHODS: Spectrophotometry was used to measure the oxidative/anti-oxidative indices including malonyldialdehyed (MDA) and GSH in the kidney of MRL/lpr lupus mice. Quantitative PCR and Western blotting were used to detected the expression of γ-GCS. RESULTS: The level of GSH was lowered whereas the level of MDA increased significantly in the kidney tissue of MRL/lpr lupus mice as compared with that in normal control mice. The expression of γ-GCS mRNA and protein was significantly decreased in MRL/lpr lupus mice (P<0.05). CONCLUSION: MRL/lpr lupus mice have abnormal oxidative stress in the kidney tissue, where the expression of γ-GCS decreased to lead to reduced GSH production, damaged antioxidative capacity, and eventually exacerbation of oxidative damage in the kidney.