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sle, trfhisgtg, tlr, nets, pevs, formation, neutrophils, pubmed, patients, fig, article, activation, google, scholar, lupus, evs, production, ics, levels, inhibitor, human, platelets, cas, increased, systemic, extracellular, control, disease, cells, usa, erythematosus, release, presence, central, induced, expression, tsrnas, net, shown, assay, immune, study, min, effect, dna, activity, mimic, vesicles, induce, taichung,

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induced il-1β/il-8/interferon-α upregulation ic-primed platelet-derived trf ics-primed platelet-derived trf sle-derived low-density granulocytes tsai-ling liao nf-κb-mediated cytokines/chemokines platelet-derived extracellular vesicles lupus-prone transgenic mice trna-derived rna fragments ics-triggered nets formation tlr8-specific antagonist cu-cpt9a il-1β/il-8/ifnα production article download pdf systemic lupus erythematosus sle patient-derived ics platelet-released extracellular vesicles extracellular-signal-regulated kinase mitogen-activated protein kinase platelet-derived ssrna carried specific 2’-o-methyl modification sle patient-derived pevs tlr8-specific inhibitor cu-cpt9a human platelet-derived evs hek-htlr8 cell model ev-specific surface markers inflammatory cytokines/ifnα production enzyme-linked immunosorbent assay ic-triggered trf sle patient-derived neutrophils infection-induced 5′-half molecules virus-induced exosomal micrornas gtg-1-induced nets formation hung-jen liu kuo-tung tang slow-fade mounting medium gtg-1–induced net formation hek-blue htlr8 cells regulate nf-κb activity upregulated platelet-derived trf real-time pcr quantification hc subject-derived pevs trna-derived fragments sle ics-induced pevs alix [alg-2-interacting protein induce ifn-α production derived small rnas nets formation/ hyperactivation nets formation/hyperactivation trf-val-aac-1-m7 sle pevs-induced nets

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         headline:tRF-His-GTG-1 enhances NETs formation and interferon-α production in lupus by extracellular vesicle
         description:Hyperactive neutrophil extracellular traps (NETs) formation plays a crucial role in active severe systemic lupus erythematosus (SLE). However, what triggers the imbalance in dysregulated NETs formation in SLE is elusive. Transfer RNA-derived small RNAs (tsRNAs) are novel non-coding RNAs, which participate in various cellular processes. We explore the role of tsRNAs on NETs formation in SLE. We analyzed the levels of NETs DNA and platelet-derived extracellular vesicles (pEVs) from 50 SLE patients and 20 healthy control subjects. The effects of pEVs on NETs formation were evaluated by using immunofluorescence assay and myeloperoxidase-DNA PicoGreen assay. The regulatory mechanism of pEVs on NETs formation and inflammatory cytokines production were investigated using an in vitro cell-based assay. Increased circulating NETs DNA and pEVs were shown in SLE patients and were associated with disease activity (P < 0.005). We demonstrated that SLE patient-derived immune complexes (ICs) induced platelet activation, followed by pEVs release. ICs-triggered NETs formation was significantly enhanced in the presence of pEVs through Toll-like receptor (TLR) 8 activation. Increased levels of tRF-His-GTG-1 in pEVs and neutrophils of SLE patients were associated with disease activity. tRF-His-GTG-1 interacted with TLR8 to prime p47phox phosphorylation in neutrophils, resulting in reactive oxygen species production and NETs formation. Additionally, tRF-His-GTG-1 modulated NF-κB and IRF7 activation in neutrophils upon TLR8 engagement, resulting IL-1β, IL-8, and interferon-α upregulation, respectively. The level of tRF-His-GTG-1 was positively correlated with NETs formation in SLE patients; tRF-His-GTG-1 inhibitor could efficiently suppress ICs-triggered NETs formation/hyperactivation, which may become a potential therapeutic target. Neutrophils and platelets are key members in the immunopathogenesis of SLE. EVs play a key role in intercellular communication. Abnormal NETs formation promotes vascular complications and organ damage in SLE patients. tsRNA is a novel regulatory small non-coding RNA and participates in diverse pathological processes. Herein, we showed that SLE patient-derived ICs activates platelets directly, followed by intracellular tRF-His-GTG-1 upregulation, which is loaded into pEVs. The pEV-carried tRF-His-GTG-1 could interact with TLR8 in neutrophils, followed by activation of the downstream signaling pathway, including p47phox-NOX2-ROS, which causes NETs enhancement, while IRF7 promotes the expression of IFN-α. The tRF-His-GTG-1 inhibitor could suppress efficiently SLE ICs-induced NETs formation and pEVs primed NETs enhancement. This study offers new molecular machinery to explain the association between the platelets-derived tsRNAs, pEVs, and hyperactive NETs formation in lupus. tRF-His-GTG-1 may serve as a potential therapeutic target and help to advance our understanding of tsRNAs in SLE pathogenesis.
         datePublished:2024-07-07T00:00:00Z
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            Platelet
            Extracellular vesicles
            tRNA-derived small RNA
            Neutrophil extracellular traps
            Interferon-α
            Cell Biology
            Protein-Ligand Interactions
            Receptors
            Cytokines and Growth Factors
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      headline:tRF-His-GTG-1 enhances NETs formation and interferon-α production in lupus by extracellular vesicle
      description:Hyperactive neutrophil extracellular traps (NETs) formation plays a crucial role in active severe systemic lupus erythematosus (SLE). However, what triggers the imbalance in dysregulated NETs formation in SLE is elusive. Transfer RNA-derived small RNAs (tsRNAs) are novel non-coding RNAs, which participate in various cellular processes. We explore the role of tsRNAs on NETs formation in SLE. We analyzed the levels of NETs DNA and platelet-derived extracellular vesicles (pEVs) from 50 SLE patients and 20 healthy control subjects. The effects of pEVs on NETs formation were evaluated by using immunofluorescence assay and myeloperoxidase-DNA PicoGreen assay. The regulatory mechanism of pEVs on NETs formation and inflammatory cytokines production were investigated using an in vitro cell-based assay. Increased circulating NETs DNA and pEVs were shown in SLE patients and were associated with disease activity (P < 0.005). We demonstrated that SLE patient-derived immune complexes (ICs) induced platelet activation, followed by pEVs release. ICs-triggered NETs formation was significantly enhanced in the presence of pEVs through Toll-like receptor (TLR) 8 activation. Increased levels of tRF-His-GTG-1 in pEVs and neutrophils of SLE patients were associated with disease activity. tRF-His-GTG-1 interacted with TLR8 to prime p47phox phosphorylation in neutrophils, resulting in reactive oxygen species production and NETs formation. Additionally, tRF-His-GTG-1 modulated NF-κB and IRF7 activation in neutrophils upon TLR8 engagement, resulting IL-1β, IL-8, and interferon-α upregulation, respectively. The level of tRF-His-GTG-1 was positively correlated with NETs formation in SLE patients; tRF-His-GTG-1 inhibitor could efficiently suppress ICs-triggered NETs formation/hyperactivation, which may become a potential therapeutic target. Neutrophils and platelets are key members in the immunopathogenesis of SLE. EVs play a key role in intercellular communication. Abnormal NETs formation promotes vascular complications and organ damage in SLE patients. tsRNA is a novel regulatory small non-coding RNA and participates in diverse pathological processes. Herein, we showed that SLE patient-derived ICs activates platelets directly, followed by intracellular tRF-His-GTG-1 upregulation, which is loaded into pEVs. The pEV-carried tRF-His-GTG-1 could interact with TLR8 in neutrophils, followed by activation of the downstream signaling pathway, including p47phox-NOX2-ROS, which causes NETs enhancement, while IRF7 promotes the expression of IFN-α. The tRF-His-GTG-1 inhibitor could suppress efficiently SLE ICs-induced NETs formation and pEVs primed NETs enhancement. This study offers new molecular machinery to explain the association between the platelets-derived tsRNAs, pEVs, and hyperactive NETs formation in lupus. tRF-His-GTG-1 may serve as a potential therapeutic target and help to advance our understanding of tsRNAs in SLE pathogenesis.
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         Systemic lupus erythematosus
         Platelet
         Extracellular vesicles
         tRNA-derived small RNA
         Neutrophil extracellular traps
         Interferon-α
         Cell Biology
         Protein-Ligand Interactions
         Receptors
         Cytokines and Growth Factors
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      name:Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
      name:Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung, Taiwan
      name:Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
      name:Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung, Taiwan
      name:Ph.D. Program in Translational Medicine, National Chung Hsing University, Taichung, Taiwan
      name:Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan
      name:The iEGG and Animal Biotechnology Center, National Chung Hsing University, Taichung, Taiwan
      name:Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
      name:Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan
      name:Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung, Taiwan
      name:Ph.D. Program in Translational Medicine, National Chung Hsing University, Taichung, Taiwan

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