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      MicroRNAs as regulators of metabolic disease: pathophysiologic significance and emerging role as biomarkers and therapeutics

      review-article
      Author(s): 1 , *
      Publication date (Electronic):
      Journal: International Journal of Obesity (2005)
      Publisher: Nature Publishing Group

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          Abstract

          The prevalence of overweight and obesity in developed and developing countries has greatly increased the risk of insulin resistance and type 2 diabetes mellitus. It is evident from human and animal studies that obesity alters microRNA (miRNA) expression in metabolically important organs, and that miRNAs are involved in changes to normal physiology, acting as mediators of disease. miRNAs regulate multiple pathways including insulin signaling, immune-mediated inflammation, adipokine expression, adipogenesis, lipid metabolism, and food intake regulation. Thus, miRNA-based therapeutics represent an innovative and attractive treatment modality, with non-human primate studies showing great promise. In addition, miRNA measures in plasma or bodily fluids may be used as disease biomarkers and predictors of metabolic disease in humans. This review analyzes the role of miRNAs in obesity and insulin resistance, focusing on the miR-17/92, miR-143-145, miR-130, let-7, miR-221/222, miR-200, miR-223, miR-29 and miR-375 families, as well as miRNA changes by relevant tissue (adipose, liver and skeletal muscle). Further, the current and future applications of miRNA-based therapeutics and diagnostics in metabolic disease are discussed.

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          Origins and Mechanisms of miRNAs and siRNAs.

          Richard W. Carthew, Erik J. Sontheimer (2009)
          Over the last decade, approximately 20-30 nucleotide RNA molecules have emerged as critical regulators in the expression and function of eukaryotic genomes. Two primary categories of these small RNAs--short interfering RNAs (siRNAs) and microRNAs (miRNAs)--act in both somatic and germline lineages in a broad range of eukaryotic species to regulate endogenous genes and to defend the genome from invasive nucleic acids. Recent advances have revealed unexpected diversity in their biogenesis pathways and the regulatory mechanisms that they access. Our understanding of siRNA- and miRNA-based regulation has direct implications for fundamental biology as well as disease etiology and treatment.
          Article 0 comments Cited 1536 times – based on 0 reviews     Review now
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            Posttranscriptional regulation of the heterochronic gene lin-14 by lin-4 mediates temporal pattern formation in C. elegans.

            Bruce Wightman, Ilho Ha, Gary Ruvkun (1993)
            During C. elegans development, the temporal pattern of many cell lineages is specified by graded activity of the heterochronic gene Lin-14. Here we demonstrate that a temporal gradient in Lin-14 protein is generated posttranscriptionally by multiple elements in the lin-14 3'UTR that are regulated by the heterochronic gene Lin-4. The lin-14 3'UTR is both necessary and sufficient to confer lin-4-mediated posttranscriptional temporal regulation. The function of the lin-14 3'UTR is conserved between C. elegans and C. briggsae. Among the conserved sequences are seven elements that are each complementary to the lin-4 RNAs. A reporter gene bearing three of these elements shows partial temporal gradient activity. These data suggest a molecular mechanism for Lin-14p temporal gradient formation: the lin-4 RNAs base pair to sites in the lin-14 3'UTR to form multiple RNA duplexes that down-regulate lin-14 translation.
            Article 0 comments Cited 1066 times – based on 0 reviews     Review now
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              miR-145 and miR-143 Regulate Smooth Muscle Cell Fate Decisions

              Kimberly Cordes, Neil T. Sheehy, Mark White … (2009)
              SUMMARY microRNAs are regulators of myriad cellular events, but evidence for a single microRNA that can efficiently differentiate multipotent cells into a specific lineage or regulate direct reprogramming of cells into an alternate cell fate has been elusive. Here, we show that miR-145 and miR-143 are co-transcribed in multipotent cardiac progenitors before becoming localized to smooth muscle cells, including neural crest stem cell–derived vascular smooth muscle cells. miR-145 and miR-143 were direct transcriptional targets of serum response factor, myocardin and Nkx2.5, and were downregulated in injured or atherosclerotic vessels containing proliferating, less differentiated smooth muscle cells. miR-145 was necessary for myocardin-induced reprogramming of adult fibroblasts into smooth muscle cells and sufficient to induce differentiation of multipotent neural crest stem cells into vascular smooth muscle. Furthermore, miR-145 and miR-143 cooperatively targeted a network of transcription factors, including Klf4, myocardin, and Elk-1 to promote differentiation and repress proliferation of smooth muscle cells. These findings demonstrate that miR-145 can direct the smooth muscle fate and that miR-145 and miR-143 function to regulate the quiescent versus proliferative phenotype of smooth muscle cells.
              Article 0 comments Cited 458 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Obes (Lond)
                Journal ID (iso-abbrev): Int J Obes (Lond)
                Title: International Journal of Obesity (2005)
                Publisher: Nature Publishing Group
                ISSN (Print): 0307-0565
                ISSN (Electronic): 1476-5497
                Publication date (Print): January 2016
                Publication date (Electronic preprint): 27 August 2015
                Publication date (Electronic): 29 September 2015
                Volume: 40
                Issue: 1
                Pages: 88-101
                Affiliations
                [1 ]Department of Medicine, University of Maryland Baltimore , Baltimore, MD, USA
                Author notes
                [* ]Department of Medicine, University of Maryland Baltimore , 20 Penn Street, Health Sciences Facility II Rm S012C, Baltimore, MD 21201, USA. E-mail: jdeiuliis@ 123456medicine.umaryland.edu
                Article
                Publisher Item ID: ijo2015170
                DOI: 10.1038/ijo.2015.170
                PMC ID: 4722234
                PubMed ID: 26311337
                SO-VID: 02fe8266-a77d-48a4-b975-87766962dd68
                Copyright © Copyright © 2016 Macmillan Publishers Limited
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                Date received : 08 January 2015
                Date revision received : 01 July 2015
                Date accepted : 22 July 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics

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