IGJ depletion suppresses proliferation, inflammation, and motility of rheumatoid arthritis fibroblast-like synoviocytes via targeting NF-κB pathway.

OBJECTIVE: To investigate the impact of IGJ on the proliferation, inflammation, and motility of rheumatoid arthritis (RA) fibroblast-like synoviocytes and elucidate the underlying mechanism. METHODS: The expression of IGJ RA fibroblast-like synoviocytes was assessed using immunoblot and qPCR. Cell growth was evaluated using CCK-8 and FCM assays. The effects on inflammatory response were determined by ELISA and immunoblot assays. Cell motility was assessed using transwell and immunoblot assays. The mechanism was further confirmed using immunoblot assays. RESULTS: IGJ expression was found to be elevated in fibroid synovial cells of RA. IGJ ablation inhibited the growth of MH7A cells and suppressed the inflammatory response. Knockdown of IGJ also blocked cell motility. Mechanically, the knockdown of IGJ suppressed the NF-κB axis in MH7A cells. CONCLUSION: IGJ suppresses RA in fibroblast-like synoviocytes via NF-κB pathway.

Causal association between rheumatoid arthritis and risk of stroke: A Mendelian randomization study.

BACKGROUND: Active rheumatoid arthritis (RA) may damage vascular endothelial cells, thereby increasing the likelihood of adverse cardiovascular events. However, it is not yet clearly established whether RA also increases the risk of adverse cerebrovascular events, particularly stroke. OBJECTIVE: This study was designed to evaluate the likelihood of a causal association between RA and stroke. METHOD: A two-sample Mendelian randomization (MR) analysis was performed using the inverse variance-weighted (IVW) average, weighted median, and MR-Egger regression methods. The analysis utilized publicly available summary statistics datasets from Genome-wide association studies (GWAS) meta-analyses for RA in individuals of European descent (total n = 484,598; case = 5427, control = 479,171) as the exposure cohort, and from GWAS meta-analyses for "vascular/heart problems diagnosed by doctor: stroke" in individuals included in the UK Biobank (total n = 461,880; case = 7055, control = 454,825, MRC-IEU consortium) as the outcome cohort. RESULTS: Eight single-nucleotide polymorphisms with genome-wide significance were selected from the GWASs on RA as the instrumental variables. The results of the MR-Egger and weighted median analyses showed no causal association between RA and stroke (OR = 1.081, 95 % CI [0.943-1.240], P = 0.304) vs. OR = 1.079, 95 % CI [0.988-1.179], P = 0.091), respectively. However, the inverse variance-weighted (IVW) analysis results revealed a causal association between RA and stroke (OR = 1.115, 95 % CI [1.040-1.194], P = 0.002). Cochran's Q test and MR-Egger regression revealed no evidence of heterogeneity and horizontal pleiotropy. CONCLUSION: The MR analysis results indicated that rheumatoid arthritis (RA) may be causally associated with an increased risk of stroke.

Neuromyelitis in a Patient with Rheumatoid Arthritis: A Case Report.

A patient with longstanding rheumatoid arthritis (RA) complained of spinal cord symptoms after RA relapse. Contrast MRI demonstrated neuromyelitis in the upper thoracic spinal cord, and anti-aquaporin-4 (anti-AQP4) antibody was positive in the serum and cerebrospinal fluid (CSF). Neuromyelitis optica spectrum disorder (NMOSD) was diagnosed after excluding central nervous system (CNS) infection and tumor, and spinal cord symptoms were relieved after high dose of glucocorticoid and immunosuppressant were initiated for treatment.

Relationship between plasma fibrinogen degradation products(FDP) and D-dimer levels and disease activity in rheumatoid arthritis: A STROBE compliant article.

In this study, we aimed to investigate whether fibrinogen degradation products(FDP)and D-dimer could be used as serological indicators of rheumatoid arthritis(RA) activity, such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and platelets (PLT). A total of 112 consecutive patients with RA between July 2018 and July 2020 were divided into moderate and high disease activity groups (disease activity score 28(DAS28) > 3.2, n = 60) and low disease activity and remission groups (DAS28≤3.2, n = 52). A total of 50 healthy volunteers were included in the control group, and FDP and D-dimer levels were compared across the three groups. The correlations of FDP and D-dimer levels with ESR, CRP, PLT, and DAS28 were analyzed. Analyses of the receiver operating characteristic(ROC) curves and area under the ROC curve (AUC) of FDP, D-dimer, ESR, CRP, and PLT levels were performed. FDP and D-dimer levels were significantly higher in the high-activity compared to the low-activity and remission (P < .001), and the control (P < .001). No significant differences in FDP and D-dimer were observed between the low-activity and remission and the control (P > .05). FDP and D-dimer levels were positively correlated with ESR, CRP, PLT, and DAS28 (all P < .001). The ROC curves showed that the FDP and D-dimer levels could be used to evaluate the RA activity (all P < .001). The AUC of FDP was significantly larger than that of PLT (P = .047). FDP and D-dimer can be used as supplementary serological indicators to assess RA activity, in addition to ESR, CRP, and PLT.

Association of long non-coding RNA GAS5 and miR-21 levels in CD4+ T cells with clinical features of systemic lupus erythematosus.

The present study aimed to assess the expression of growth arrest-specific 5 (GAS5) and microRNA (miR)-21 in systemic lupus erythematosus (SLE), and attempted to explore their association with clinical features. CD4+ T cells were isolated from peripheral blood of healthy donors and SLE patients by magnetic-activated cell sorting. GAS5 and miR-21 expression levels in cluster of differentiation (CD)4+ T cells were measured by reverse-transcription quantitative polymerase chain reaction. The results revealed that GAS5 and miR-21 levels were significantly elevated in CD4+ T cells of patients with SLE compared with those in control subjects (P<0.05). Regarding clinical features, SLE patients with ulceration had higher GAS5 expression levels in CD4+ T cells than those without ulceration (P<0.05), and the expression of miR-21 was significantly higher in CD4+ T cells of SLE patients with low levels of complement component 3 (C3) than in those with normal levels of complement C3 (P<0.05). In conclusion, GAS5 and miR-21 in CD4+ T cells may serve as potential biomarkers for the diagnosis and monitoring of the progression of SLE.