Question: Which micro-RNAs have been associated in the pathogenesis of Rheumatoid Arthritis?

Context:
This study provides the first description of increased expression of miRNA miR-155 and miR-146a in RA
In this study we investigated the expression, regulation, and function of miR-155 and miR-146a in rheumatoid arthritis (RA) synovial fibroblasts (RASFs) and RA synovial tissue
The objective of this study was to identify the expression pattern of microRNA-146 (miR-146) in synovial tissue from patients with rheumatoid arthritis (RA)
This study shows that miR-146 is expressed in RA synovial tissue and that its expression is induced by stimulation with TNFalpha and IL-1beta
pregulated miR-146a expression in peripheral blood mononuclear cells from rheumatoid arthritis patients
Total RNA was isolated from peripheral blood mononuclear cells obtained from patients with rheumatoid arthritis, and healthy and disease control individuals, and the expression of miR-146a, miR-155, miR-132, miR-16, and microRNA let-7a was analyzed using quantitative real-time PCR
Rheumatoid arthritis peripheral blood mononuclear cells exhibited between 1.8-fold and 2.6-fold increases in miR-146a, miR-155, miR-132, and miR-16 expression, whereas let-7a expression was not significantly different compared with healthy control individuals
Our data also suggest a possible mechanism contributing to rheumatoid arthritis pathogenesis, whereby miR-146a expression is increased but unable to properly function, leading to prolonged tumor necrosis factor-alpha production in patients with rheumatoid arthritis
Repression of TRAF6 and/or IRAK-1 in THP-1 cells resulted in up to an 86% reduction in tumor necrosis factor-alpha production, implicating that normal miR-146a function is critical for the regulation of tumor necrosis factor-alpha production
icroRNA-124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast-like synoviocytes from patients with rheumatoid arthritis
We found that miR-124a levels significantly decreased in RA synoviocytes as compared with OA synoviocytes
Induction of miR-124a in RA synoviocytes significantly suppressed the production of the CDK-2 and MCP-1 proteins
he results of this study suggest that miR-124a is a key miRNA in the posttranscriptional regulatory mechanisms of RA synoviocytes
iR-223 is overexpressed in T-lymphocytes of patients affected by rheumatoid arthritis.
Although a multifactorial pathogenesis has been hypothesized, the precise mechanisms leading to the disease are still poorly understood at the molecular level. miRNA expression profile analysis highlighted that miR-223 is the only miRNA that is strikingly deregulated in peripheral T-lymphocytes from RA patients compared with healthy donors
In summary, our data provide a first characterization of the miRNA expression profiles of peripheral T-lymphocytes of RA patients, identifying miR-223 as overexpressed in CD4(+) naive T-lymphocytes from these individuals
Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid arthritis
The role of miR-146a overexpression in regulating T cell apoptosis was evaluated by flow cytometry
We have detected increased miR-146a in CD4+ T cells of RA patients and its close correlation with TNF-alpha levels. Our findings that miR-146a overexpression suppresses T cell apoptosis indicate a role of miR-146a in RA pathogenesis and provide potential novel therapeutic targets
icroRNA-146a expresses in interleukin-17 producing T cells in rheumatoid arthritis patients
Six miRNAs, let-7a, miR-26, miR-146a/b, miR-150, and miR-155 were significantly up regulated in the IL-17 producing T cells
These results indicated that miR-146a was associated with IL-17 expression in the PBMC and synovium in RA patients
polymorphism in the 3'-UTR of interleukin-1 receptor-associated kinase (IRAK1), a target gene of miR-146a, is associated with rheumatoid arthritis susceptibility
MicroRNA-146a was found to be increased in synovial fibroblasts, synovial tissue and PBMC from patients with RA
This is the first study that addresses association of a variant in a target of miR-146a, IRAK1 gene, with RA susceptibility
ltered expression of microRNA-203 in rheumatoid arthritis synovial fibroblasts and its role in fibroblast activation
Previously, we described increased expression of miR-155 and miR-146a in rheumatoid arthritis (RA) and showed a repressive effect of miR-155 on matrix metalloproteinase (MMP) expression in RA synovial fibroblasts (RASFs)
The current results demonstrate methylation-dependent regulation of miR-203 expression in RASFs
 Importantly, they also show that elevated levels of miR-203 lead to increased secretion of MMP-1 and IL-6 via the NF-κB pathway and thereby contribute to the activated phenotype of synovial fibroblasts in RA
iR-124a as a key regulator of proliferation and MCP-1 secretion in synoviocytes from patients with rheumatoid arthritis
Transfection of miR-124a into RA synoviocytes significantly suppressed their proliferation and arrested the cell cycle at the G1 phase
It is proposed that miR-124a is a key miRNA in the post-transcriptional regulatory mechanisms of RA synoviocytes, and has a therapeutic potential
Expression of miR-146a and miR-16 in peripheral blood mononuclear cells of patients with rheumatoid arthritis and their correlation to the disease activity
The elevated expression levels of miR-146a and miR-16 are correlated to RA disease activity, suggesting their value in assessment of the clinical disease activity of RA
iR-346 controls release of TNF-α protein and stability of its mRNA in rheumatoid arthritis via tristetraprolin stabilization
Using a microarray, we found two miRNAs, miR-125b and miR-939 predicted to target the 3'-UTR of TNF-α mRNA, to be up-regulated in RA FLS in response to LPS, but their repression did not restore mature TNF-α expression in FLS
We showed previously that miR-346, which is upregulated in LPS-activated FLS, inhibited Btk expression that stabilized TNF-α mRNA
Different expression patterns of mir-146a, miRNA-155, miRNA-124a, mir-203, mir-223, mir-346, mir-132, mir-363, mir-498, mir-15a, and mir-16 were documented in several tissue sample types of RA patients
own-regulation of microRNA-34a* in rheumatoid arthritis synovial fibroblasts promotes apoptosis resistance
Basal expression levels of miR-34a* were found to be reduced in synovial fibroblasts from RA patients compared to osteoarthritis patients, whereas levels of miR-34a, miR-34b/b*, and miR-34c/c* did not differ
Our data provide evidence of a methylation-specific down-regulation of proapoptotic miR-34a* in RASFs
dentification of microRNA-221/222 and microRNA-323-3p association with rheumatoid arthritis via predictions using the human tumour necrosis factor transgenic mouse model
miR-seq demonstrated that TghuTNF-SF exhibit a distinct pathogenic profile with 22 significantly upregulated and 30 significantly downregulated miR
Validation assays confirmed the dysregulation of miR-223, miR-146a and miR-155 previously associated with human rheumatoid arthritis (RA) pathology, as well as that of miR-221/222 and miR-323-3p
the authors identified miR-221/222 and miR-323-3p as novel dysregulated miR in RA SF
Further association studies may contribute to determining the role of miR-146a single-nucleotide polymorphisms in immune-mediated diseases
iR-146a polymorphism is associated with asthma but not with systemic lupus erythematosus and juvenile rheumatoid arthritis in Mexican patients.
verexpression of microRNA-223 in rheumatoid arthritis synovium controls osteoclast differentiation
MicroRNA-223 (miR-223) is reported to play critical roles in osteoclastogenesis
MiR-223 is intensely expressed in RA synovium, and overexpression of miR-223 suppresses osteoclastogenesis in vitro
This study demonstrates the possibility of gene therapy with miR-223 to treat bone destruction in RA patients
MiR-223 was more highly expressed in RA synovium than in osteoarthritis (OA) synovium due to the increased number of miR-223-positive cells in RA synovium
ssociation of pre-miRNA-146a rs2910164 and pre‑miRNA-499 rs3746444 polymorphisms and susceptibility to rheumatoid arthritis
Our findings demonstrated that the hsa-mir-499 rs3746444, but not mir-146a rs2910164, polymorphism is associated with an increased RA risk in a sample of the Iranian population
umor necrosis factor α-induced microRNA-18a activates rheumatoid arthritis synovial fibroblasts through a feedback loop in NF-κB signaling
To elucidate whether the microRNA (miRNA) cluster miR-17-92 contributes to the activated phenotype of rheumatoid arthritis synovial fibroblasts (RASFs
We found that TNFα induces the expression of miR-17-92 in RASFs in an NF-κB-dependent manner
Using reporter gene assays, we identified the NF-κB pathway inhibitor TNFα-induced protein 3 as a new target of miR-18a
Our data suggest that the miR-17-92-derived miR-18a contributes to cartilage destruction and chronic inflammation in the joint through a positive feedback loop in NF-κB signaling, with concomitant up-regulation of matrix-degrading enzymes and mediators of inflammation in RASFs
As inflammation and joint damage are the main hallmarks of RA, we focused on the three miRNAs, miR-146a, miR-155 and miR-223, whose functions have been studied in both the processes and the pathogenic role investigated in the experimental models
Focusing on the role of miR-146a, miR-155 and miR-223 in RA pathogenesis emphasizes the intertwined relationships between bone homeostasis and immunity, and the prominent role of monocytes in RA
In a final perspective section we discuss the potential impact of therapeutic miR-155 modulation in RA
correlation between whole blood and PBMC expression levels of miR-155 and miR-146a in healthy controls and rheumatoid arthritis patients
We demonstrated a highly significant linear correlation between miR-146a and miR-155 expression in PBMC and whole blood, from both healthy individuals and RA patients.
expression of specific microRNAs (miRNA) in peripheral blood-derived mononuclear cells (PBMC), particularly miR-146a and miR-155, is associated with rheumatoid arthritis (RA)
icroRNA-323-3p with clinical potential in rheumatoid arthritis, Alzheimer's disease and ectopic pregnancy
It has been shown that miR-323-3p associates with the pathogenesis of several diseases, such as rheumatoid arthritis, Alzheimer's disease and ectopic pregnancy

Answer: Different expression patterns of mir-146a, miRNA-155, miRNA-124a, mir-203, mir-223, mir-346, mir-132, mir-363, mir-498, mir-15a, and mir-16 were documented in several tissue sample types of RA patients.
Exact answer: miR-155, miR-146a, miR-124a, miR-222, miR-223, miR-203, miR-346, miR-132, miR-363, miR-498, miR-15a, miR-16, miR-18a