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      MicroRNAs as Potential Signatures of Environmental Exposure or Effect: A Systematic Review

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      Author(s): 1 , 2 , 1 , 3 ,
      Publication date (Electronic):
      Journal: Environmental Health Perspectives
      Publisher: NLM-Export

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          Abstract

          Background: The exposome encompasses all life-course environmental exposures from the prenatal period onward that influence health. MicroRNAs (miRNAs) are interesting entities within this concept as markers and causation of disease. MicroRNAs are short oligonucleotide sequences that can interact with several mRNA targets.

          Objectives: We reviewed the current state of the field on the potential of using miRNAs as biomarkers for environmental exposure. We investigated miRNA signatures in response to all types of environmental exposure to which a human can be exposed, including cigarette smoke, air pollution, nanoparticles, and diverse chemicals; and we examined the health conditions for which the identified miRNAs have been reported (i.e., cardiovascular disease, cancer, and diabetes).

          Methods: We searched the PubMed and ScienceDirect databases to identify relevant studies.

          Results: For all exposures incorporated in this review, 27 miRNAs were differentially expressed in at least two independent studies. miRNAs that had expression alterations associated with smoking observed in multiple studies are miR-21, miR-34b, miR-125b, miR-146a, miR-223, and miR-340; and those miRNAs that were observed in multiple air pollution studies are miR-9, miR-10b, miR-21, miR-128, miR-143, miR-155, miR-222, miR-223, and miR-338. We found little overlap among in vitro, in vivo, and human studies between miRNAs and exposure. Here, we report on disease associations for those miRNAs identified in multiple studies on exposure.

          Conclusions: miRNA changes may be sensitive indicators of the effects of acute and chronic environmental exposure. Therefore, miRNAs are valuable novel biomarkers for exposure. Further studies should elucidate the role of the mediation effect of miRNA between exposures and effect through all stages of life to provide a more accurate assessment of the consequences of miRNA changes.

          Citation: Vrijens K, Bollati V, Nawrot TS. 2015. MicroRNAs as potential signatures of environmental exposure or effect: a systematic review. Environ Health Perspect 123:399–411;  http://dx.doi.org/10.1289/ehp.1408459

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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.
          Article 0 comments Cited 850 times – based on 0 reviews     Review now
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            MiR-150 controls B cell differentiation by targeting the transcription factor c-Myb.

            Changchun Xiao, Dinis Calado, Gunther Galler … (2007)
            MiR-150 is a microRNA (miRNA) specifically expressed in mature lymphocytes, but not their progenitors. A top predicted target of miR-150 is c-Myb, a transcription factor controlling multiple steps of lymphocyte development. Combining loss- and gain-of-function gene targeting approaches for miR-150 with conditional and partial ablation of c-Myb, we show that miR-150 indeed controls c-Myb expression in vivo in a dose-dependent manner over a narrow range of miRNA and c-Myb concentrations and that this dramatically affects lymphocyte development and response. Our results identify a key transcription factor as a critical target of a stage-specifically expressed miRNA in lymphocytes and suggest that this and perhaps other miRNAs have evolved to control the expression of just a few critical target proteins in particular cellular contexts.
            Article 0 comments Cited 322 times – based on 0 reviews     Review now
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              MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice.

              Andrew H Williams, Gregorio Valdez, Viviana Moresi … (2009)
              Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons, denervation of target muscles, muscle atrophy, and paralysis. Understanding ALS pathogenesis may require a fuller understanding of the bidirectional signaling between motor neurons and skeletal muscle fibers at neuromuscular synapses. Here, we show that a key regulator of this signaling is miR-206, a skeletal muscle-specific microRNA that is dramatically induced in a mouse model of ALS. Mice that are genetically deficient in miR-206 form normal neuromuscular synapses during development, but deficiency of miR-206 in the ALS mouse model accelerates disease progression. miR-206 is required for efficient regeneration of neuromuscular synapses after acute nerve injury, which probably accounts for its salutary effects in ALS. miR-206 mediates these effects at least in part through histone deacetylase 4 and fibroblast growth factor signaling pathways. Thus, miR-206 slows ALS progression by sensing motor neuron injury and promoting the compensatory regeneration of neuromuscular synapses.
              Article 0 comments Cited 276 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (iso-abbrev): Environ. Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: NLM-Export
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 16 January 2015
                Publication date (Print): May 2015
                Volume: 123
                Issue: 5
                Pages: 399-411
                Affiliations
                [1 ]Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium
                [2 ]Center of Molecular and Genetic Epidemiology, Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
                [3 ]Department of Public Health and Primary Care, Environment and Health Unit, Leuven Univeristy, Leuven, Belgium
                Author notes
                Address correspondence to T.S. Nawrot, Centre for Environmental Sciences, Hasselt University, Agoralaan Gebouw D, B-3590 Diepenbeek, Belgium. Telephone: 32-11-268382. E-mail: tim.nawrot@ 123456uhasselt.be
                Article
                Publisher ID: ehp.1408459
                DOI: 10.1289/ehp.1408459
                PMC ID: 4421768
                PubMed ID: 25616258
                SO-VID: 77d3ee0d-3809-4366-a2a4-ab01a44ab4a7
                License:

                Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, “Reproduced with permission from Environmental Health Perspectives”); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.

                History
                Date received : 22 March 2014
                Date accepted : 14 January 2015
                Date: 16 January 2015
                Date: 01 May 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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