The expression of GAS5, THRIL, and RMRP lncRNAs is increased in T cells of patients with rheumatoid arthritis

Moharamoghli, Mozhgan; Hassan‐Zadeh, Vahideh; Dolatshahi, Elahe; Alizadeh, Zahra; Farazmand, Ali

doi:10.1007/s10067-019-04694-z

Cited by 59 publications

(40 citation statements)

References 39 publications

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“…The overexpression of lncRNA THRIL in patients with inflammatory‐related diseases is reported by several studies . For example, it is reported that lncRNA THRIL is highly expressed in rheumatoid arthritis (RA) patients compared to healthy controls and discriminates RA patients from controls . Meanwhile, in multiple sclerosis patients, lncRNA THRIL is overexpressed compared to healthy subjects .…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Shen

Zhou

2020

Clinical Laboratory Analysis

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractObjective: This study aimed to investigate the role of long non-coding RNA (lncRNA) THRIL in coronary heart disease (CHD) patients. Methods:A total of 420 patients who underwent coronary arteriography due to suspected symptoms of CHD were enrolled, in which 220 were diagnosed as CHD and 200 were set as control subjects. LncRNA THRIL in plasma samples of CHD patients

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Section: Discussionmentioning

confidence: 99%

Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Shen

Zhou

2020

Clinical Laboratory Analysis

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“…In T cells from patients with RA, compared with their expression in healthy controls, the lncRNAs LOC100652951, LOC100506036 [ 68 ], THRIL, and RMRP [ 69 ] are upregulated. RA patients treated with biological agents such as abatacept and tocilizumab show lower expression levels of LOC100652951.…”

Section: Important Roles Of Lncrnas In Autoimmune Diseasesmentioning

confidence: 99%

“… [ 67 ] LOC100652951, LOC100506036 Human T cell Up-regulated Regulates inflammation response. [ 68 ] GAS5, THRIL, RMRP Human T cell Up-regulated – [ 69 ] H19 Human Synovial tissue, FLS, macrophage Up-regulated Induced by serum starvation and under control of PI3K and ERK pathway. [ 74 ] LERFS Human Synovial tissue, FLS Down-regulated Regulates migration, invasion and proliferation by interacting with hnRNPQ.…”

Section: Introductionmentioning

confidence: 99%

Involvement of long noncoding RNAs in the pathogenesis of autoimmune diseases

Zou

2020

Journal of Translational Autoimmunity

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Autoimmune diseases are a group of heterogeneous disorders characterized by damage to various organs caused by abnormal innate and adaptive immune responses. The pathogenesis of autoimmune diseases is extremely complicated and has not yet been fully elucidated. Long noncoding RNAs (lncRNAs), which are defined as transcripts containing more than 200 nucleotides with no protein-coding capacity, are emerging as important regulators of gene expression via epigenetic modification, transcriptional regulation and posttranscriptional regulation. Accumulating evidence has demonstrated that lncRNAs play a key role in the regulation of immunological functions and autoimmunity. In this review, we discuss various molecular mechanisms by which lncRNAs regulate gene expression and recent findings regarding the involvement of lncRNAs in many human autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), idiopathic inflammatory myopathy (IIM), systemic sclerosis (SSc) and Sjögren’s syndrome (pSS).

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“…In recent years, many LncRNAs have attracted much attention from scientists based on their involvement in mediating cell apoptosis, signal transduction, metabolism and immune response 14 . For example, LncRNA‐CMPK2, 15 LincRNA‐Cox2, 16 LncRNA MALAT1, 17 LncRNA ZFAS1, 18 TUG1, 19 LncRNA‐NR024118 20 and LncRNA growth arrest‐specific transcript5 (GAS5) 21 are closely related to autoimmune dysfunction of peripheral blood mononuclear cells (PBMCs), T and B lymphocytes as well as synovial fibroblasts 22 . Similarly, Song et al 23 confirmed LncRNA Hotair as a novel biomarker by regulating matrix metalloproteinase (MMP)‐2 and MMP‐13 expressions in osteoclasts and synovial cells of RA patients.…”

Section: Introductionmentioning

confidence: 99%

LncRNA GAS5 activates the AMPK pathway in peripheral blood mononuclear cells derived from rheumatoid arthritis patients

Cao

Zhang

et al. 2020

Int J of Rheum Dis

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Rheumatoid arthritis (RA) is an inflammatory disease characterized by destruction of synovial joints, 1 abnormal immune responses 2 and inflammatory manifestations, 3 which seriously affects human joints. 4 Although much progress has been made in the development of effective drugs for RA, the disease-associated disability rate is still high. Genetical studies have shown that rheumatoid factors 5 and a variety of inflammatory processes 6 play an important role in the mechanism of RA, albeit the etiology of the disease still not understood.

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The expression of GAS5, THRIL, and RMRP lncRNAs is increased in T cells of patients with rheumatoid arthritis

Cited by 59 publications

References 39 publications

Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Involvement of long noncoding RNAs in the pathogenesis of autoimmune diseases

LncRNA GAS5 activates the AMPK pathway in peripheral blood mononuclear cells derived from rheumatoid arthritis patients

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