Analysis of lncRNA expression profiles by sequencing reveals that lnc-AL928768.3 and lnc-AC091493.1 are novel biomarkers for disease risk and activity of rheumatoid arthritis
“…Regarding the majority of RA patients, biological therapies are highly effective. Until now, the pathogenesis of RA is not fully known, but some clinical studies have found that long non-coding RNAs (lncRNAs), which are non-protein-coding RNAs (>200 nucleotides in length), may be involved [12,13].…”
Objective: Long non-coding RNAs (lncRNAs) and their target microRNAs were documented in multiple studies to have a significant role in different joint disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA). The current work aimed to determine the potential role of lnc-PVT1 and miR-146a as promising biomarkers to distinguish between RA, OA patients, and healthy individuals. Methods: The expression levels of lnc-PVT1 and its target miR-146a in the serum were measured for three different groups, including patients with RA (40), OA patients (40), and healthy controls (HCs) (40). Participating individuals were subjected to a full history investigation and clinical examination. Blood samples were tested for ESR, RF, CBC, as well as liver and renal functions. Serum was used to detect the relative expression levels of lnc-PVT1 and miR-146a and we correlated the levels with RA and OA activity and severity signs. Results: Lnc-PVT1 expression level was greater among patients with RA compared to that of OA patients, with a fold change median of 2.62 and 0.22, respectively (p = 0.001). The miR-146a fold change was significantly demonstrated between the RA, OA, and HCs groups. There was no correlation between both biomarkers with the disease activity scales (DAS28) of RA, the Knee injury Osteoarthritis Outcome Score (KOOS), or any sign of detection of the disease severity of OA. Conclusions: lnc-PVT1 and miR-146a could be considered as promising biomarkers for the diagnosis of RA and OA and may have an important role as therapeutic targets in the future.
“…Regarding the majority of RA patients, biological therapies are highly effective. Until now, the pathogenesis of RA is not fully known, but some clinical studies have found that long non-coding RNAs (lncRNAs), which are non-protein-coding RNAs (>200 nucleotides in length), may be involved [12,13].…”
Objective: Long non-coding RNAs (lncRNAs) and their target microRNAs were documented in multiple studies to have a significant role in different joint disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA). The current work aimed to determine the potential role of lnc-PVT1 and miR-146a as promising biomarkers to distinguish between RA, OA patients, and healthy individuals. Methods: The expression levels of lnc-PVT1 and its target miR-146a in the serum were measured for three different groups, including patients with RA (40), OA patients (40), and healthy controls (HCs) (40). Participating individuals were subjected to a full history investigation and clinical examination. Blood samples were tested for ESR, RF, CBC, as well as liver and renal functions. Serum was used to detect the relative expression levels of lnc-PVT1 and miR-146a and we correlated the levels with RA and OA activity and severity signs. Results: Lnc-PVT1 expression level was greater among patients with RA compared to that of OA patients, with a fold change median of 2.62 and 0.22, respectively (p = 0.001). The miR-146a fold change was significantly demonstrated between the RA, OA, and HCs groups. There was no correlation between both biomarkers with the disease activity scales (DAS28) of RA, the Knee injury Osteoarthritis Outcome Score (KOOS), or any sign of detection of the disease severity of OA. Conclusions: lnc-PVT1 and miR-146a could be considered as promising biomarkers for the diagnosis of RA and OA and may have an important role as therapeutic targets in the future.
“…In addition, lnc-AL928768.3 and lnc-AC091493.1 increased in RA patients compared with the control group, and these two lncRNAs were positively correlated with ESR, CRP levels and disease activity scores (Sun et al, 2020b). lnc-AL928768.3 and lnc-AC091493.1 may be new markers of RA risk and disease severity.…”
Section: Lncrnas Involved In the Pathogenesis Of Rheumatoid Arthritismentioning
Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology, mainly manifested by persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), inflammation, synovial hyperplasia and cartilage erosion, accompanied by joint swelling and joint destruction. Abnormal expression or function of long noncoding RNAs (lncRNAs) are closely related to human diseases, including cancers, mental diseases, autoimmune diseases and others. The abnormal sequence and spatial structure of lncRNAs, the disorder expression and the abnormal interaction with the binding protein will lead to the change of gene expression in the way of epigenetic modification. Increasing evidence demonstrated that lncRNAs were involved in the activation of FLSs, which played a key role in the pathogenesis of RA. In this review, the research progress of lncRNAs in the pathogenesis of RA was systematically summarized, including the role of lncRNAs in the diagnosis of RA, the regulatory mechanism of lncRNAs in the pathogenesis of RA, and the intervention role of lncRNAs in the treatment of RA. Furthermore, the activated signal pathways, the role of DNA methylation and other mechanism have also been overview in this review.
“…Some studies have proven that lncRNA expression is related to the risk and activity of RA. In addition, lncRNAs can participate in the regulation of relevant signaling pathways in order to affect FLS proliferation ( 48 , 49 ). In a previously published study, it was verified that lncRNA LOC100912373 is a differentially expressed gene that is crucial for the occurrence and development of RA; in addition, lncRNA LOC100912373 can induce FLS proliferation by competing with miR-17-5p, so as to promote PDK1/AKT signaling pathway activation, thereby promoting RA progression ( 24 ).…”
Previous studies have confirmed that astragaloside (AST) exerts a positive effect on alleviating synovial and joint injury in rheumatoid arthritis (RA). However, the precise mechanisms through which AST acts in the treatment of RA remain unclear. Long non-coding RNA (lncRNA) LOC100912373 was identified as a key gene related to RA and has been proven to interact with miR-17-5p, in order to regulate the pyruvate dehydrogenase kinase 1 and protein kinase B axis (PDK1/AKT axis). The present study aimed to determine whether AST may treat RA through the interaction between lncRNA LOC100912373 and the miR-17-5p/PDK1 axis. MTT assays and flow cytometry were used to detect the proliferation and cell cycle progression of AST-treated fibroblast-like synoviocytes (FLSs). The expression of lncRNA LOC100912373 and miR-17-5p, as well as relative the mRNA expression of the PDK1 and AKT genes following AST intervention was detected by reverse transcription-quantitative PCR (RT-qPCR), immunofluorescence and western blot analysis. The results revealed that AST inhibited FLS proliferation, reduced lncRNA LOC100912373 expression levels, increased miR-17-5p expression levels, and decreased the PDK1 and p-AKT expression levels. Additionally, consecutive rescue experiments revealed that AST counteracted the effects of lncRNA LOC100912373 overexpression on FLS proliferation and cell cycle progression. On the whole, the present study demonstrates that AST inhibits FLS proliferation by regulating the expression of lncRNA LOC100912373 and the miR-17-5p/PDK1 axis.
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