Overexpression of long noncoding RNA LINC00638 inhibits inflammation and oxidative stress in rheumatoid arthritis fibroblast‐like synoviocytes by regulating the Nrf2/HO‐1 pathway

Sun, Yanqiu; Liu, Jian; Wen, Jianting; Huang, Dan; Zhou, Qin; Zhang, Xianheng; Ding, Xiang; Chen, Xiaolu

doi:10.1002/iid3.663

Cited by 9 publications

(4 citation statements)

References 41 publications

(66 reference statements)

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“…Cell purity was assessed by flow cytometry (Becton, Dickinson and Company, Franklin Lakes, NJ). Cells at generations 3 to 5 were selected for following experiments, and FLS for negative control (NCFLS, HUMiCells010; iCell Bioscience, Shanghai, China) were incubated in DMEM supplemented with 10% FBS (sh30256.01; Hyclone) 16 …”

Section: Methodsmentioning

confidence: 99%

LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast‐like synoviocyte in rheumatoid arthritis

Wang,

Xu,

Zhang

et al. 2024

The Kaohsiung J of Med Scie

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Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, and the role of HOXA transcript at the distal tip (HOTTIP) in its pathogenesis remains underexplored. This study investigates the mechanism by which HOTTIP influences apoptosis and the inflammatory response of fibroblast‐like synoviocytes (FLS). An RA mouse model was established, and clinical scores were analyzed. Pathological changes in synovial tissues, bone mineral density (BMD) of the paws, serum tartrate‐resistant acid phosphatase (TRAP) activity, and TNF‐α and IL‐1β levels were assessed. FLS were transfected, and cell proliferation and apoptosis were examined. The RNA‐pull‐down assay determined HOTTIP's interaction with mixed‐lineage leukemia 1 (MLL1), while RNA immunoprecipitation assay measured HOTTIP expression pulled down by MLL1. The levels of MLL1 and toll‐like receptor 4 (TLR4) after MLL1 overexpression based on HOTTIP silencing were determined. Chromatin immunoprecipitation (ChIP) was performed with H3K4me3 as an antibody, followed by the evaluation of TLR4 expression. HOTTIP expression was elevated in RA mouse synovial tissues. Inhibition of HOTTIP led to reduced clinical scores, inflammatory infiltration, synovial hyperplasia, TRAP activity, and TNF‐α and IL‐1β levels, along with increased BMD. In vitro Interference with HOTTIP suppressed RA‐FLS apoptosis and inflammation. HOTTIP upregulated TLR4 expression by recruiting MLL1 to facilitate TLR4 promoter methylation. MLL1 overexpression reversed HOTTIP silencing‐mediated repression of RA‐FLS apoptosis. Activation of H3K4 methylation counteracted HOTTIP knockout, ameliorating the inflammatory response. HOTTIP regulates TLR4 expression by recruiting MLL1, leading to TLR4 promoter methylation, thereby suppressing RA‐FLS proliferation and inducing cell apoptosis and inflammatory response in RA.

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Section: Methodsmentioning

confidence: 99%

LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast‐like synoviocyte in rheumatoid arthritis

Wang,

Xu,

Zhang

et al. 2024

The Kaohsiung J of Med Scie

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“…RA is one of the most common and highly heterogeneous autoimmune diseases associated with a considerable increase in disability and mortality ( 216 ). Delayed diagnosis is one of the most critical problems in RA management.…”

Section: Conclusion and Future Outlookmentioning

confidence: 99%

Biomarkers (mRNAs and non-coding RNAs) for the diagnosis and prognosis of rheumatoid arthritis

Jiang

Zhong

et al. 2023

Front. Immunol.

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In recent years, diagnostic and therapeutic approaches for rheumatoid arthritis (RA) have continued to improve. However, in the advanced stages of the disease, patients are unable to achieve long-term clinical remission and often suffer from systemic multi-organ damage and severe complications. Patients with RA usually have no overt clinical manifestations in the early stages, and by the time a definitive diagnosis is made, the disease is already at an advanced stage. RA is diagnosed clinically and with laboratory tests, including the blood markers C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) and the autoantibodies rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPA). However, the presence of RF and ACPA autoantibodies is associated with aggravated disease, joint damage, and increased mortality, and these autoantibodies have low specificity and sensitivity. The etiology of RA is unknown, with the pathogenesis involving multiple factors and clinical heterogeneity. The early diagnosis, subtype classification, and prognosis of RA remain challenging, and studies to develop minimally invasive or non-invasive biomarkers in the form of biofluid biopsies are becoming more common. Non-coding RNA (ncRNA) molecules are composed of long non-coding RNAs, small nucleolar RNAs, microRNAs, and circular RNAs, which play an essential role in disease onset and progression and can be used in the early diagnosis and prognosis of RA. In this review of the diagnostic and prognostic approaches to RA disease, we provide an overview of the current knowledge on the subject, focusing on recent advances in mRNA–ncRNA as diagnostic and prognostic biomarkers from the biofluid to the tissue level.

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“…lncRNA FAO regulates inflammation in macrophage cells followed by restoration of homeostasis by activating fatty acid oxidation via its interaction with the HADHB subunit of the mitochondrial trifunctional protein for FAO activation ( Nakayama et al, 2020 ). Zhao et al, in 2022 showed that lncRNA Carl is an apoptosis-related lncRNA; during intestinal inflammation, the expression or overexpression of the lncRNA Carl leads to the expression of IL-1 beta and of the ptgs2 gene via its interaction with NF-kB P65; lncRNA CHRF leads to an increase in cytokine and oxidant levels following its overexpression, it also triggers the inflammation signaling pathway by activating MyD88 through miR-489; lncRNA FIRRE acts at the post-transcriptional level to regulate proinflammatory genes by interacting with hnRNPU proteins and by binding to the p56 subunit of NFkB; lncRNA PTPRE-AS1 acts via the MAPK/ERK1/2 signaling pathway to regulate inflammation via increasing and decreasing levels of TNF-alpha and IL-10 respectively; Long intergenic RNA not encoding proteins 638 (Linc00638) is implicated in several autoimmune diseases ( Yanqiu et al, 2022 ). It regulates oxidative stress and inflammation especially by targeting inflammatory cytokines like IL-6, IL-17, IL-23 and regulating the Nrf2HO-1 pathway in rheumatoid arthritis ( Sun et al, 2021 ).…”

Section: Non-coding Rnas Involved In Oxidative Stress and Inflammatio...mentioning

confidence: 99%

An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders

et al. 2023

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Oxidative stress is a state in which oxidants are produced in excess in the body’s tissues and cells, resulting in a biological imbalance amid the generation of reactive oxygen and nitrogen species (RONS) from redox reactions. In case of insufficient antioxidants to balance, the immune system triggers signaling cascades to mount inflammatory responses. Oxidative stress can have deleterious effects on major macromolecules such as lipids, proteins, and nucleic acids, hence, Oxidative stress and inflammation are among the multiple factors contributing to the etiology of several disorders such as diabetes, cancers, and cardiovascular diseases. Non-coding RNAs (ncRNAs) which were once referred to as dark matter have been found to function as key regulators of gene expression through different mechanisms. They have dynamic roles in the onset and development of inflammatory and oxidative stress-related diseases, therefore, are potential targets for the control of those diseases. One way of controlling those diseases is through the use of natural products, a rich source of antioxidants that have drawn attention with several studies showing their involvement in combating chronic diseases given their enormous gains, low side effects, and toxicity. In this review, we highlighted the natural products that have been reported to target ncRNAs as mediators of their biological effects on oxidative stress and several inflammation-associated disorders. Those natural products include Baicalein, Tanshinone IIA, Geniposide, Carvacrol/Thymol, Triptolide, Oleacein, Curcumin, Resveratrol, Solarmargine, Allicin, aqueous extract or pulp of Açai, Quercetin, and Genistein. We also draw attention to some other compounds including Zanthoxylum bungeanum, Canna genus rhizome, Fuzi-ganjiang herb pair, Aronia melanocarpa, Peppermint, and Gingerol that are effective against oxidative stress and inflammation-related disorders, however, have no known effect on ncRNAs. Lastly, we touched on the many ncRNAs that were found to play a role in oxidative stress and inflammation-related disorders but have not yet been investigated as targets of a natural product. Shedding more light into these two last points of shadow will be of great interest in the valorization of natural compounds in the control and therapy of oxidative stress- and inflammation-associated disorders.

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Overexpression of long noncoding RNA LINC00638 inhibits inflammation and oxidative stress in rheumatoid arthritis fibroblast‐like synoviocytes by regulating the Nrf2/HO‐1 pathway

Cited by 9 publications

References 41 publications

LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast‐like synoviocyte in rheumatoid arthritis

LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast‐like synoviocyte in rheumatoid arthritis

Biomarkers (mRNAs and non-coding RNAs) for the diagnosis and prognosis of rheumatoid arthritis

An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders

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