microRNA-99a Restricts Replication of Hepatitis C Virus by Targeting mTOR and De Novo Lipogenesis

Lee, Eun Byul; Sung, Pil Soo; Kim, Jung-Hee; Park, Dong-Jun; Hur, Wonhee; Yoon, Shin Hee

doi:10.3390/v12070696

Cited by 12 publications

(9 citation statements)

References 24 publications

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“…Previous studies have revealed that miR-99a functions by targeting on mammalian target of rapamycin (mTOR) 19 , 27 and that mTOR is a pivotal regulator of T cell differentiation and glycolysis. 24 , 28 We therefore explored whether mTOR is involved in miR-99a-regulated CD4 + T cell differentiation and glycolysis.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have revealed that miR-99a functions by targeting the mRNAs of genes, such as mTOR, NOX4, HOXA1, and KDM6B. 19 , 27 , 38 , 39 , 40 Among those target genes, mTOR is well-known to regulate CD4 + T cell differentiation and glycolysis. 24 , 28 Consistently, our bioinformatics analysis showed that mTOR was a target for miR-99a in CD4 + T cells.…”

Section: Discussionmentioning

confidence: 99%

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miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

Yang

et al. 2021

Molecular Therapy - Nucleic Acids

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Multiple microRNAs exhibit diverse functions to regulate inflammatory and autoimmune diseases. MicroRNA-99a (miR-99a) has been shown to be involved in adipose tissue inflammation and to be downregulated in the inflammatory lesions of autoimmune diseases rheumatoid arthritis and systemic lupus erythematosus. In this study, we found that miR-99a was downregulated in CD4 + T cells from experimental autoimmune encephalomyelitis (EAE) mice, an animal model of multiple sclerosis. Overexpression of miR-99a alleviated EAE development by promoting regulator T cells and inhibiting T helper type 1 (Th1) cell differentiation. Bioinformatics and functional analyses further revealed that the anti-inflammatory effects of miR-99a was attributable to its role in negatively regulating glycolysis reprogramming of CD4 + T cells by targeting the mTOR pathway. Additionally, miR-99a expression was induced by transforming growth factor β (TGF-β) to regulate CD4 + T cell glycolysis and differentiation. Taken together, our results characterize a pivotal role of miR-99a in regulating CD4 + T cell differentiation and glycolysis reprogramming during EAE development, which may indicate that miR-99a is a promising therapeutic target for the amelioration of multiple sclerosis and possibly other autoimmune diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

Yang

et al. 2021

Molecular Therapy - Nucleic Acids

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“…The expression of miR-99a was significantly lower in patients with chronic HCV infection than in healthy subjects. miR-99a modulates the expression of the mammalian target of rapamycin protein (mTOR) to improve intracellular lipid accumulation and limit HCV replication [ 57 ]. miR-200c, which is increased in HCV-infected patients, regulates the Src kinase signaling pathway and promotes liver fibrosis by directly targeting Fas-associated phosphatase 1 (FAP-1), a negative regulator of Src signaling [ 60 ].…”

Section: Association Of the Causes Of Liver Cirrhosis And Mirnasmentioning

confidence: 99%

Diagnosis and Therapeutic Management of Liver Fibrosis by MicroRNA

Tadokoro

Morishita

Masaki

2021

IJMS

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Remarkable progress has been made in the treatment and control of hepatitis B and C viral infections. However, fundamental treatments for diseases in which liver fibrosis is a key factor, such as cirrhosis, alcoholic/nonalcoholic steatohepatitis, autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, are still under development and remain an unmet medical need. To solve this problem, it is essential to elucidate the pathogenesis of liver fibrosis in detail from a molecular and cellular perspective and to develop targeted therapeutic agents based on this information. Recently, microRNAs (miRNAs), functional RNAs of 22 nucleotides, have been shown to be involved in the pathogenesis of liver fibrosis. In addition, extracellular vesicles called “exosomes” have been attracting attention, and research is being conducted to establish noninvasive and extremely sensitive biomarkers using miRNAs in exosomes. In this review, we summarize miRNAs directly involved in liver fibrosis, miRNAs associated with diseases leading to liver fibrosis, and miRNAs related to complications of cirrhosis. We will also discuss the efficacy of each miRNA as a biomarker of liver fibrosis and pathology, and its potential application as a therapeutic agent.

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“…The signal transducer and activator of transcription (STAT) signaling pathways play an important role in viral infection, such as immune regulation and apoptosis 18,19 . The mammalian target of rapamycin (mTOR) signaling pathway is one of the major cell signaling pathways in viral infection 20,21 . The aim of the present study is to validate how DAPP inhibit EV71 to induce the apoptosis of Vero cell and provide a potential pharmaceutical against the infection of EV71 virus.…”

Section: Introductionmentioning

confidence: 98%

The inhibition of enterovirus 71 induced apoptosis by Durvillaea antarctica through P53 and STAT1 signaling pathway

et al. 2020

Journal of Medical Virology

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The infection of enterovirus 71 (EV71) resulted in hand, foot, and mouth disease and may lead to severe nervous system damage and even fatalities. There are no effective drugs to treat the EV71 virus and it is crucial to find novel drugs against it. Polysaccharide isolated from Durvillaea antarctica green algae has an antiviral effect. In this study, D. antarctica polysaccharide (DAPP) inhibited the infection of EV71 was demonstrated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), reverse transcription polymerase chain reaction, flow cytometry, and western blot. MTT assay showed that DAPP had no toxicity on Vero cells at the concentration 250 μg/ml. Furthermore, DAPP significantly reduced the RNA level of EV71 in a dose‐dependent manner. Moreover, DAPP inhibited the Vero cells apoptosis induced by EV71 via the P53 signaling pathway. Meanwhile, the expression of signal transducer and activator of transcription 1 and mammalian target of rapamycin were increased and the proinflammatory cytokines were significantly inhibited by DAPP. Taken together, these results suggested that DAPP could be a potential pharmaceutical against the infection of EV71 virus.

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microRNA-99a Restricts Replication of Hepatitis C Virus by Targeting mTOR and De Novo Lipogenesis

Cited by 12 publications

References 24 publications

miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

Diagnosis and Therapeutic Management of Liver Fibrosis by MicroRNA

The inhibition of enterovirus 71 induced apoptosis by Durvillaea antarctica through P53 and STAT1 signaling pathway

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