Evidence map›Paper›PMID 29269398›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018

MiR-184 expression is regulated by AMPK in pancreatic islets.

Aida Martinez-Sanchez, Marie-Sophie Nguyen-Tu, Ines Cebola, Arash Yavari, Piero Marchetti, Lorenzo Piemonti, Eelco de Koning, A M James Shapiro, Paul Johnson, Kei Sakamoto and 5 more

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Liver kinase B1 (LKB1) regulates the epigenetic landscape of mouse pancreatic beta cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  11. The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 10 institutions in 8 countries.

Aida Martinez-SanchezSection of Cell Biology and Functional Genomics Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Marie-Sophie Nguyen-TuSection of Cell Biology and Functional Genomics Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Ines CebolaBeta Cell Genome Regulation Laboratory, Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Arash YavariRadcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Piero MarchettiDepartment of Endocrinology and Metabolism, University of Pisa, Pisa, Italy.
Lorenzo PiemontiSan Raffaele Diabetes Research Institute (SR-DRI), Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Milan, Italy.
Eelco de KoningHubrecht Institute, Utrecht, The Netherlands.
A M James ShapiroClinical Islet Laboratory and Clinical Islet Transplant Program, University of Alberta, Edmonton, Alberta, Canada.
Paul JohnsonNuffield Department of Surgical Sciences, University of Oxford, Oxford, United Kingdom.
Kei SakamotoNestle Institute of Health Sciences, Lausanne, Switzerland.
David M SmithAstraZeneca Research and Development, Innovative Medicines and Early Development, Discovery Sciences, Cambridge, United Kingdom.
Isabelle LeclercSection of Cell Biology and Functional Genomics Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Houman AshrafianRadcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Jorge FerrerBeta Cell Genome Regulation Laboratory, Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Guy A RutterSection of Cell Biology and Functional Genomics Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Imperial College London, London, United Kingdom.
Genomics (United Kingdom) · GBUniversity of Pisa · ITAstraZeneca (Singapore) · SGDiabetes UK · GBGenomics England · GBHôpital Nestlé · CHHubrecht Institute for Developmental Biology and Stem Cell Research · NLIstituti di Ricovero e Cura a Carattere Scientifico · ITNuffield Orthopaedic Centre · GBUniversity of Alberta · CA

Funding

Medical Research Council MR/J0003042/1Medical Research Council MR/K001981/1Medical Research Council MR/K019023/1Medical Research Council MR/L020149/1Medical Research Council MR/L02036X/1Medical Research Council MR/N00275X/1Medical Research Council MR/P023223/1Wellcome TrustWellcome Trust WT098424AIA
6 · The paper itself

Abstract

AMPK is a critical energy sensor and target for widely used antidiabetic drugs. In β cells, elevated glucose concentrations lower AMPK activity, and the ablation of both catalytic subunits [β-cell-specific AMPK double-knockout (βAMPKdKO) mice] impairs insulin secretion in vivo and β-cell identity. MicroRNAs (miRNAs) are small RNAs that silence gene expression that are essential for pancreatic β-cell function and identity and altered in diabetes. Here, we have explored the miRNAs acting downstream of AMPK in mouse and human β cells. We identified 14 down-regulated and 9 up-regulated miRNAs in βAMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichment in pathways important for β-cell function and identity. The most down-regulated miRNA was miR-184 (miR-184-3p), an important regulator of β-cell function and compensatory expansion that is controlled by glucose and reduced in diabetes. We demonstrate that AMPK is a potent regulator and an important mediator of the negative effects of glucose on miR-184 expression. Additionally, we reveal sexual dimorphism in miR-184 expression in mouse and human islets. Collectively, these data demonstrate that glucose-mediated changes in AMPK activity are central for the regulation of miR-184 and other miRNAs in islets and provide a link between energy status and gene expression in β cells.-Martinez-Sanchez, A., Nguyen-Tu, M.-S., Cebola, I., Yavari, A., Marchetti, P., Piemonti, L., de Koning, E., Shapiro, A. M. J., Johnson, P., Sakamoto, K., Smith, D. M., Leclerc, I., Ashrafian, H., Ferrer, J., Rutter, G. A. MiR-184 expression is regulated by AMPK in pancreatic islets.

Indexed as

Gene Expression RegulationAMP-Activated Protein KinasesAnimalsCell LineDiabetes MellitusEnergy MetabolismFemaleGlucoseHumansInsulin-Secreting CellsMaleMiceMice, KnockoutMicroRNAsSex CharacteristicsAMP-Activated Protein KinasesGlucoseMicroRNAsMIRN184 microRNA, humanMIRN184 microRNA, mousediabetesglucosemiRNAsβ cell

Identifiers

PMID29269398
PMCPMC6207280
OpenAlexW2779751466

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.