MicroRNA-146a and Human Disease

Li, L.; Chen, X.-P.; Li, Y.-J.

doi:10.1111/j.1365-3083.2010.02383.x

Cited by 206 publications

(175 citation statements)

References 53 publications

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“…It participates in signaling cascade regulation associated with TLR/IL-1R, changing the expression of inflammatory factors such as tumor necrosis factor-α (TNF-α) and type I IFNs. TRAF6 is involved in the cellular immune response by interacting with TLRs and the IFN-γ signal transduction pathway Li et al, 2010b). Let-7a is upregulated by EBNA1 and has been shown to directly alter cell cycle progression and pro-inflammatory cytokine production.…”

Section: Ebv Latent Proteins Dysregulate Host Mirnas To Regulate the mentioning

confidence: 99%

“…MiR-146a also targets two immune-associated genes, interleukin-1 receptor-associated kinase 1 (IRAK1) and TNF receptorassociated factor 6 (TRAF6). IRAK1 is a key innate immune signal molecule (Li et al, 2010b;Saba et al, 2014). It participates in signaling cascade regulation associated with TLR/IL-1R, changing the expression of inflammatory factors such as tumor necrosis factor-α (TNF-α) and type I IFNs.…”

Section: Ebv Latent Proteins Dysregulate Host Mirnas To Regulate the mentioning

confidence: 99%

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An update: Epstein-Barr virus and immune evasion via microRNA regulation

Zuo

Yue

et al. 2017

Virol. Sin.

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Epstein-Barr virus (EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans.To ensure its survival and maintain its B cell transformation function, EBV has developed powerful strategies to evade host immune responses. Emerging evidence has shown that microRNAs (miRNAs) are powerful regulators of the maintenance of cellular homeostasis. In this review, we summarize current progress on how EBV utilizes miRNAs for immune evasion. EBV encodes miRNAs targeting both viral and host genes involved in the immune response. The miRNAs are found in two gene clusters, and recent studies have demonstrated that lack of these clusters increases the CD4 + and CD8 + T cell response of infected cells. These reports strongly indicate that EBV miRNAs are critical for immune evasion. In addition, EBV is able to dysregulate the expression of a variety of host miRNAs, which influence multiple immune-related molecules and signaling pathways. The transport via exosomes of EBV-regulated miRNAs and viral proteins contributes to the construction and modification of the inflammatory tumor microenvironment. During EBV immune evasion, viral proteins, immune cells, chemokines, pro-inflammatory cytokines, and pro-apoptosis molecules are involved. Our increasing knowledge of the role of miRNAs in immune evasion will improve the understanding of EBV persistence and help to develop new treatments for EBV-associated cancers and other diseases.

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Section: Ebv Latent Proteins Dysregulate Host Mirnas To Regulate the mentioning

confidence: 99%

Section: Ebv Latent Proteins Dysregulate Host Mirnas To Regulate the mentioning

confidence: 99%

An update: Epstein-Barr virus and immune evasion via microRNA regulation

Zuo

Yue

et al. 2017

Virol. Sin.

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“…miR-146a plays important roles in regulating the innate immunity and inflammatory responses (Rusca and Monticelli 2011;Ichii et al 2012). Aberrant expression of miR-146a has been observed in a variety of disease, including cancer, autoimmune and inflammatory diseases, and infectious diseases (Li et al 2010). Rs2910164 resides in the pre-miR-146 gene on human chromosome 5 and results in from a G:U pair to a C:U mismatch in the stem structure of the miR-146a precursor.…”

Section: Discussionmentioning

confidence: 99%

Association of microRNA Polymorphisms with the Risk of Myocardial Infarction in a Chinese Population

Chen

Hong

Chen

et al. 2014

Tohoku J. Exp. Med.

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MicroRNAs (miRNAs) are involved in the regulation of a variety of biological processes, such as inflammation. Dysregulation of miRNAs have been implicated in many human disease, including cardiovascular diseases. Polymorphisms in miRNA genes may affect the miRNA biogenesis and function, and thus cause changes in the expression of thousands of genes. The aim of this study was to examine whether miRNA polymorphisms (miR-146a rs2910164, miR-149 rs71428439, miR-196a2 rs11614913, miR-218 rs11134527, and miR-499 rs3746444) contribute to the risk for the development of myocardial infarction (MI). Five miRNA polymorphisms were genotyped in a total of 1808 subjects composed of 919 MI patients and 889 control individuals. The GG genotype of rs3746444 was found to be associated with a significantly increased risk of MI (recessive model, adjusted OR = 1.710, 95% CI: 1.058-2.763, P = 0.029). Although the CC genotype of rs2910164 significantly increased the risk of MI under dominant and additive models (P < 0.05), this difference disappeared after adjustment for age, sex, blood pressure, triglycerides, total cholesterol, HDL, LDL and diabetes. In addition, when rs3746444 and rs2910164 were evaluated together by the number of putative high-risk alleles, we found an increased risk of MI for subjects carrying 3-4 risk alleles (3-4 risk alleles vs. 0-1 risk allele, adjusted OR = 1.580, 95% CI: 1.069-2336, P = 0.022; 3-4 risk alleles vs. 0-2 risk allele, adjusted OR = 1.513, 95% CI: 1.031-2.219, P = 0.034). These findings indicate that miR-499 rs3746444 and miR-146a rs2910164 may represent novel markers of MI susceptibility.

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“…The miR-146a promoter contains several binding sites for nuclear factor (NF)-κB and has been shown both in vitro and in vivo to target IRAK1 and TRAF6, thus suppressing the expression of NF-κB's target genes such as IL-6, IL-8, IL-1β, and TNF-α (62,63). Therefore, miR-146a acts as an effector molecule that drives a negative feedback mechanism, able to attenuate the TLRs response (64). In contrast to miR-155 and miR-146, in macrophages miR-125b is down-regulated upon LPS stimulation (65).…”

Section: Micrornas Regulation Of Innate Immunitymentioning

confidence: 99%

Innate Immunity and Human Milk MicroRNAs Content: A New Perspective for Premature Newborns

et al. 2017

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Context: The premature newborns are prone to develop both early onset and late onset neonatal sepsis. The major causes of this phenomenon rely on the immaturity of the immune system, which has reduced capability to respond adequately to pathogens. Evidence Acquisition: Titles and abstracts of previous papers were scanned before reading the full-text, in order to retrieve appropriate information. The databases used for searching were PubMed, Cochrane, and Embase for articles published before 1st of July, 2016. Secondary search for articles cited in reference lists were identified by the primary search. This review focused on neonatal sepsis incidence and the associated immune response with regards to microRNAs of human milk as a new microelement that enables regulation of innate immunity functions. Results: Since human milk is a valuable source of microRNAs, a better understanding of its content will open a new therapeutic avenue for the clinical management of infectious diseases affecting premature newborns. The variation in miRNAs quantity in human milk needs to be considered. Mother's milk can have different amounts of miRNAs and the identification of a microMilk batch richer of miRNAs can be a nutrition intervention method for modulating innate immunity in clinical management of premature newborns. Conclusions: Routine translation of the microMilk concept for neonatal intensive care unit (NICU), in the management of premature newborns could be a way of defending premature newborns and Very Low Birth Weight (VLBW) infants from both early and late sepsis.

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MicroRNA-146a and Human Disease

Cited by 206 publications

References 53 publications

An update: Epstein-Barr virus and immune evasion via microRNA regulation

An update: Epstein-Barr virus and immune evasion via microRNA regulation

Association of microRNA Polymorphisms with the Risk of Myocardial Infarction in a Chinese Population

Innate Immunity and Human Milk MicroRNAs Content: A New Perspective for Premature Newborns

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