Long noncoding RNAs in the metabolic control of inflammation and immune disorders

Xu, Junfang; Cao, Xuetao

doi:10.1038/s41423-018-0042-y

Cited by 35 publications

(18 citation statements)

References 57 publications

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“…Intriguingly, noncoding RNAs, especially snRNAs with stem-loop structures, can trigger TLR3 activation. 33,34 These results, together with previous reports, suggest that highly enriched noncoding RNAs in L-MPs are potential ligands that activate TLR3 signaling in macrophages. L-MPs induce mitochondrial ROS to activate NLRP3 for IL-1β cleavage Although activated TLR3 signaling can upregulate IL-1β mRNA expression and lead to the translation of pro-IL-1β, the production of mature IL-1β is mediated by inflammasome-activated caspase-1, which cleaves pro-IL-1β.…”

Section: M2-like Macrophages Induced By L-mps Upregulated Il-1β Expresupporting

confidence: 77%

Macrophages reprogrammed by lung cancer microparticles promote tumor development via release of IL-1β

et al. 2019

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Despite their mutual antagonism, inflammation and immunosuppression coexist in tumor microenvironments due to tumor and immune cell interactions, but the underlying mechanism remains unclear. Previously, we showed that tumor cell-derived microparticles induce an M2 phenotype characterized by immunosuppression in tumor-infiltrating macrophages. Here, we further showed that lung cancer microparticles (L-MPs) induce macrophages to release a key proinflammatory cytokine, IL-1β, thus promoting lung cancer development. The underlying mechanism involves the activation of TLR3 and the NLRP3 inflammasome by L-MPs. More importantly, tyrosine kinase inhibitor treatment-induced L-MPs also induce human macrophages to release IL-1β, leading to a tumor-promoting effect in a humanized mouse model. These findings demonstrated that in addition to their antiinflammatory effect, L-MPs induce a proinflammatory phenotype in tumor-infiltrating macrophages, promoting the development of inflammatory and immunosuppressive tumor microenvironments.

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Section: M2-like Macrophages Induced By L-mps Upregulated Il-1β Expresupporting

confidence: 77%

Macrophages reprogrammed by lung cancer microparticles promote tumor development via release of IL-1β

et al. 2019

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“…Previous study showed that H19 could participate in the regulation of various biological processes such as cell proliferation, apoptosis and metabolism [25], and H19 was up-regulated in cirrhotic liver tissue [26]. H19 was also reported to be a lipid sensor by synergizing with polypyrimidine tract-binding protein 1 (PTBP1) to modulate hepatic metabolic homeostasis [12].…”

Section: Discussionmentioning

confidence: 99%

LncRNA-H19 promotes hepatic lipogenesis by directly regulating miR-130a/PPARγ axis in non-alcoholic fatty liver disease

Tang

Wang

et al. 2019

Bioscience Reports

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Background: As one of the most common liver disorders worldwide, non-alcoholic fatty liver disease (NAFLD) begins with the abnormal accumulation of triglyceride (TG) in the liver. Long non-coding RNA-H19 was reported to modulate hepatic metabolic homeostasis in NAFLD. However, its molecular mechanism of NAFLD was not fully clear. Methods: In vitro and in vivo models of NAFLD were established by free fatty acid (FFA) treatment of hepatocytes and high-fat feeding mice, respectively. Hematoxylin and Eosin (H&E) and Oil-Red O staining detected liver tissue morphology and lipid accumulation. Immunohistochemistry (IHC) staining examined peroxisome proliferator-activated receptor γ (PPARγ) level in liver tissues. ELISA assay assessed TG secretion. Luciferase assay and RNA pull down were used to validate regulatory mechanism among H19, miR-130a and PPARγ. The gene expression in hepatocytes and liver tissues was detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Results: H19 and PPARγ were up-regulated, while miR-130a was down-regulated in NAFLD mouse and cellular model. H&E and Oil-Red O staining indicated an increased lipid accumulation. Knockdown of H19 inhibited steatosis and TG secretion in FFA-induced hepatocytes. H19 could bind to miR-130a, and miR-130a could directly inhibit PPARγ expression. Meanwhile, miR-130a inhibited lipid accumulation by down-regulating NAFLD-related genes PPARγ, SREBP1, SCD1, ACC1 and FASN. Overexpression of miR-130a and PPARγ antagonist GW9662 inhibited lipogenesis and TG secretion, and PPARγ agonist GW1929 reversed this change induced by miR-130a up-regulation. Conclusion: Knockdown of H19 alleviated hepatic lipogenesis via directly regulating miR-130a/PPARγ axis, which is a novel mechanistic role of H19 in the regulation of NAFLD.

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“…Long non-coding RNAs (lncRNAs) are a class of transcripts (longer than 200 nucleotides in length) without the function of encoding proteins [4]. LncRNAs have been shown to play essential roles in multiple biological processes [5–7]. In recent years, increasing evidences have demonstrated that dysregulation of lncRNA is closely associated with diverse diseases including OA [8–10].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA DANCR regulates proliferation and apoptosis of chondrocytes in osteoarthritis via miR-216a-5p-JAK2-STAT3 axis

Zhang

Sun

et al. 2018

Bioscience Reports

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Osteoarthritis (OA) is one of the most common chronic joint disease. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in a variety of diseases including OA. However, the underlying mechanism of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) in OA has not been well elucidated. The expression of DANCR in cartilage tissues from OA patients was detected using quantitative real-time PCR. After cell transfection, the effects of DANCR inhibition on the proliferation, apoptosis and inflammatory factors of OA chondrocytes were detected using Cell Counting Kit-8 assay and flow cytometry assay. Novel target of DANCR was then identified through bioinformatics analysis and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The expression of DANCR was significantly increased in OA patients. Function assays demonstrated that DANCR suppression inhibited the proliferation, inflammation, and promoted apoptosis of chondrocytes cells. Additionally, DANCR regulated survival of OA chondrocytes through acting as a competitive endogenous RNA for miR-216a-5p. Furthermore, JAK2 was a direct target of miR-216a-5p, and DANCR regulated the JAK2/STAT3 signal pathway through miR-216a-5p in OA chondrocytes. In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.

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Long noncoding RNAs in the metabolic control of inflammation and immune disorders

Cited by 35 publications

References 57 publications

Macrophages reprogrammed by lung cancer microparticles promote tumor development via release of IL-1β

Macrophages reprogrammed by lung cancer microparticles promote tumor development via release of IL-1β

LncRNA-H19 promotes hepatic lipogenesis by directly regulating miR-130a/PPARγ axis in non-alcoholic fatty liver disease

Long non-coding RNA DANCR regulates proliferation and apoptosis of chondrocytes in osteoarthritis via miR-216a-5p-JAK2-STAT3 axis

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