Eukaryotic translation initiation factor 6-mediated ribosome biogenesis promotes synovial aggression and inflammation by increasing the translation of SP1 in rheumatoid arthritis.

Introduction: Fibroblast-like synoviocytes (FLSs) play critical roles in synovial inflammation and aggression in rheumatoid arthritis (RA). Here, we explored the role of eukaryotic translation initiation factor 6 (eIF6) in regulating the biological behaviors of FLSs from patients with RA.

Methods: FLSs were isolated from the synovial tissues of RA patients.

FTO-mediated RNA mA methylation regulates synovial aggression and inflammation in rheumatoid arthritis.

Fibroblast-like synoviocytes (FLS) plays an important role in synovial inflammation and joint damage in rheumatoid arthritis (RA). As the most abundant mRNA modification, N6-methyladenosine (mA) is involved in the development of various diseases; however, its role in RA remains to be defined. In this study, we reported the elevated expression of the mA demethylase fat mass and obesity-associated protein (FTO) in FLS and synovium from RA patients.

NAT10 promotes synovial aggression by increasing the stability and translation of N4-acetylated PTX3 mRNA in rheumatoid arthritis.

Objective: Recent studies indicate that N-acetyltransferase 10 (NAT10)-mediated ac4C modification plays unique roles in tumour metastasis and immune infiltration. This study aimed to uncover the role of NAT10-mediated ac4C in fibroblast-like synoviocytes (FLSs) functions and synovial immune cell infiltration in rheumatoid arthritis (RA).

Methods: FLSs were obtained from active established patients with RA.

Coptisine inhibits aggressive and proliferative actions of fibroblast like synoviocytes and exerts a therapeutic potential for rheumatoid arthritis.

Objective: Coptisine, a natural bioactive small molecular compound extracted from traditional Chinese herb Coptis chinensis, has been shown to exhibit anti-tumor effect. However, its contribution to autoimmune diseases such as rheumatoid arthritis (RA) is unknown. Here, we evaluate the effect of coptisine in controlling fibroblast-like synoviocytes (FLS)-mediated synovial proliferation and aggression in RA and further explore its underlying mechanism(s).

ALKBH5-Mediated RNA m A Methylation Regulates the Migration, Invasion, and Proliferation of Rheumatoid Fibroblast-Like Synoviocytes.

Objective: Fibroblast-like synoviocytes (FLSs) are critical for promoting joint damage in rheumatoid arthritis (RA). N -methyladenosine (m A) modification plays key roles in various diseases, but its role in the pathogenesis of RA is largely unknown. Here, we investigate increased demethylase ALKBH5 promotion of proliferation, migration, and invasion of RA FLSs via regulating JARID2 expression.

SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C.

Fibroblast-like synoviocytes (FLSs), play a key role in perpetuating synovial inflammation and bone erosion in rheumatoid arthritis (RA), however, the underlying mechanism(s) of RA FLSs activation and aggression remain unclear. Identifying endogenous proteins that selectively target FLSs is urgently needed. Here, we systematically identified that secreted modular calcium-binding protein 2 (SMOC2), was significantly increased in RA FLSs and synovial tissues.

Long Noncoding RNA HAFML Promotes Migration and Invasion of Rheumatoid Fibroblast-like Synoviocytes.

The aggressive phenotype exhibited by fibroblast-like synoviocytes (FLSs) is critical for the progression of joint destruction in rheumatoid arthritis (RA). Long noncoding RNAs (lncRNAs) have crucial roles in the pathogenesis of diverse disorders; however, few have been identified that might be able to control the joint damage in RA. In this study, we identified an lncRNA, ENST00000509194, which was expressed at abnormally high levels in FLSs and synovial tissues from patients with RA.

signaling in the regulation of rheumatoid synovial aggression.

Background: Fibroblast-like synoviocytes (FLSs) play a critical role in promoting synovial aggression and joint destruction in rheumatoid arthritis (RA). Cyclic GMP-AMP synthase ()/stimulator of interferon gene () signaling plays an important role in controlling a series of cellular biological processes. However, it is still unclear whether signaling regulates rheumatoid synovial aggression.

The suppression of Brd4 inhibits peripheral plasma cell differentiation and exhibits therapeutic potential for systemic lupus erythematosus.

The mechanisms that control B cell terminal differentiation remain undefined. Here, we investigate the role of bromodomain-containing protein 4 (Brd4) in regulating B cell differentiation and its therapeutic potential for B cell-mediated autoimmune diseases including systemic lupus erythematosus (SLE). We showed that Brd4 inhibitor PFI-1 suppressed plasmablast-mediated plasma cell differentiation in healthy human CD19 B cells.

Increased long noncoding RNA LINK-A contributes to rheumatoid synovial inflammation and aggression.

Fibroblast-like synoviocytes (FLSs) play a key role in controlling synovial inflammation and joint destruction in rheumatoid arthritis (RA). The contribution of long noncoding RNAs (lncRNAs) to RA is largely unknown. Here, we show that the lncRNA LINK-A, located mainly in cytoplasm, has higher-than-normal expression in synovial tissues and FLSs from patients with RA.

Nitidine chloride inhibits fibroblast like synoviocytes-mediated rheumatoid synovial inflammation and joint destruction by targeting KCNH1.

Objective: Nitidine chloride (NC), a natural small molecular compound from traditional Chinese herbal medicine zanthoxylum nitidum, has been shown to exhibit anti-tumor effect. However, its role in autoimmune diseases such as rheumatoid arthritis (RA) is unknown. Here, we investigate the effect of NC in controlling fibroblast-like synoviocytes (FLS)-mediated synovial inflammation and joint destruction in RA and further explore its underlying mechanism(s).

Increased SUMO-activating enzyme SAE1/UBA2 promotes glycolysis and pathogenic behavior of rheumatoid fibroblast-like synoviocytes.

Fibroblast-like synoviocytes (FLSs) are critical to joint inflammation and destruction in rheumatoid arthritis (RA). Increased glycolysis in RA FLSs contributes to persistent joint damage. SUMOylation, a posttranslational modification of proteins, plays an important role in initiation and development of many diseases.

Accumulation of cytosolic dsDNA contributes to fibroblast-like synoviocytes-mediated rheumatoid arthritis synovial inflammation.

The accumulation of cytosolic dsDNA plays important roles in the regulation of cellular processes. However, whether cytosolic dsDNA is involved in the pathogenesis of rheumatoid arthritis (RA) is not clear. Therefore, the present study investigated the roles of cytosolic dsDNA in the modulation of inflammatory responses of fibroblast-like synoviocytes (FLS) in patients with RA.

A Multichannel Time-Tagged Time-Resolved (TTTR) Model for Quantification of Oligomer Concentrations Based on Antibunching Effect.

Molecule/protein aggregation causes many devastating and incurable diseases in human bodies. For example, studies have revealed that protein oligomers formed at the early stage are toxic and may be mostly responsible for some diseases. In the fundamental research, differentiation of different protein oligomers and quantification of the concentrations are important and challenging.

Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.

Objective: Hydroxychloroquine (HCQ) is an antimalarial drug that is widely used in the treatment of some autoimmune diseases. In the present study, we explore the role of HCQ in regulating endothelial inflammation and its underlying mechanism.

Methods: Human umbilical vein endothelial cells (HUVECs) were isolated from fresh umbilical cords.

Bio-distribution and bio-availability of silver and gold in rat tissues with silver/gold nanorod administration.

Along with the increasing applications of nanomaterials in medical fields, to know the systemic distribution of nanomaterials in the body through a precise method is required for the biosafety assessment of nanomaterials. In this study, we firstly have established a reliable inductively coupled plasma mass spectrometry (ICP-MS) method for concentration measurement of silver (Ag) and gold (Au) in biological tissues. Then, based on this method, the Ag or Au distribution in rat blood and almost all of the organs were analyzed after an i.

Quantitative deconvolution of autocorrelations and cross correlations from two-dimensional lifetime decay maps in fluorescence lifetime correlation spectroscopy.

Fluorescence correlation spectroscopy (FCS) is a widely used method for measuring molecular diffusion and chemical kinetics. However, when a mixture of fluorescent species is taken into account, the conventional FCS method has limitations in extracting autocorrelations for different species and cross correlations between different species. Recently developed fluorescence lifetime correlation spectroscopy (FLCS) based on time-tagged time-resolved (TTTR) photon recording, which can record the global and micro arrival time for each individual photon, has been used to discriminate different species according to fluorescence lifetime.

Effects of lüfukang capsules on coronary artery ligation-induced arrhythmia in dogs.

Objective: To observe the effects of Lüfukang Capsules on arrhythmia induced by ligation of coronary artery in dogs.

Methods: Thirty dogs were randomly divided into 5 groups, the model group administrated with equal volume of distilled water, the positive control group administrated with Wenxin Granules, and the small, medium and large dosage LFKC groups, 6 dogs in each group. Thirty minutes after medication, electrocardiogram was conducted and the time of arrhythmia occurrence, times of ventricular premature beat (VP), and incidence rates of ventricular tachycardia (VT) and ventricular fibrillation (VF) were recorded in the model dogs with arrhythmia induced by ligation of coronary artery.