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      Nutrimiromics: Role of microRNAs and Nutrition in Modulating Inflammation and Chronic Diseases

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          Abstract

          Nutrimiromics studies the influence of the diet on the modification of gene expression due to epigenetic processes related to microRNAs (miRNAs), which may affect the risk for the development of chronic diseases. miRNAs are a class of non-coding endogenous RNA molecules that are usually involved in post-transcriptional gene silencing by inducing mRNA degradation or translational repression by binding to a target messenger RNA. They can be controlled by environmental and dietary factors, particularly by isolated nutrients or bioactive compounds, indicating that diet manipulation may hold promise as a therapeutic approach in modulating the risk of chronic diseases. This review summarizes the evidence regarding the influence of nutrients and bioactive compounds on the expression of miRNAs related to inflammation and chronic disease in several models (cell culture, animal models, and human trials).

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Switching from repression to activation: microRNAs can up-regulate translation.

            Shobha Vasudevan, Yingchun Tong, Joan Steitz (2007)
            AU-rich elements (AREs) and microRNA target sites are conserved sequences in messenger RNA (mRNA) 3' untranslated regions (3'UTRs) that control gene expression posttranscriptionally. Upon cell cycle arrest, the ARE in tumor necrosis factor-alpha (TNFalpha) mRNA is transformed into a translation activation signal, recruiting Argonaute (AGO) and fragile X mental retardation-related protein 1 (FXR1), factors associated with micro-ribonucleoproteins (microRNPs). We show that human microRNA miR369-3 directs association of these proteins with the AREs to activate translation. Furthermore, we document that two well-studied microRNAs-Let-7 and the synthetic microRNA miRcxcr4-likewise induce translation up-regulation of target mRNAs on cell cycle arrest, yet they repress translation in proliferating cells. Thus, activation is a common function of microRNPs on cell cycle arrest. We propose that translation regulation by microRNPs oscillates between repression and activation during the cell cycle.
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              Gene silencing by microRNAs: contributions of translational repression and mRNA decay.

              Eric Huntzinger, Elisa Izaurralde (2011)
              Despite their widespread roles as regulators of gene expression, important questions remain about target regulation by microRNAs. Animal microRNAs were originally thought to repress target translation, with little or no influence on mRNA abundance, whereas the reverse was thought to be true in plants. Now, however, it is clear that microRNAs can induce mRNA degradation in animals and, conversely, translational repression in plants. Recent studies have made important advances in elucidating the relative contributions of these two different modes of target regulation by microRNAs. They have also shed light on the specific mechanisms of target silencing, which, although it differs fundamentally between plants and animals, shares some common features between the two kingdoms.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (iso-abbrev): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 27 October 2017
                Publication date Collection: November 2017
                Volume: 9
                Issue: 11
                Electronic Location Identifier: 1168
                Affiliations
                [1 ]Nutritional Genomics and Inflammation Laboratory, Department of Nutrition, School of Public Health, University of São Paulo, 01246-904 São Paulo, Brazil; bquinta@ 123456hotmail.com
                [2 ]Nutrition and Minerals Laboratory, Department of Food and Experimental Nutrition, University of São Paulo, 05508-000 São Paulo, Brazil; brunazreis@ 123456yahoo.com.br (B.Z.R.); graziela.biude@ 123456gmail.com (G.B.S.D.); smfcozzo@ 123456usp.br (S.M.F.C.)
                [3 ]Food Research Center (FoRC), 05508-000 São Paulo, Brazil
                Author notes
                [* ]Correspondence: mmrogero@ 123456usp.br ; Tel.: +55-11-30617850
                Author information
                https://orcid.org/0000-0001-8726-8699
                https://orcid.org/0000-0003-0517-1645
                Article
                Publisher ID: nutrients-09-01168
                DOI: 10.3390/nu9111168
                PMC ID: 5707640
                PubMed ID: 29077020
                SO-VID: 5a57f3ff-f0b6-476f-85ce-c4b36f3a912f
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 04 October 2017
                Date accepted : 23 October 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: microrna,nutrients,inflammation,epigenetic
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: microrna, nutrients, inflammation, epigenetic

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