Evidence map›Paper›PMID 31918917›Full record

ArticleMolecular metabolism2020

MiR-132 controls pancreatic beta cell proliferation and survival through Pten/Akt/Foxo3 signaling.

Hassan Mziaut, Georg Henniger, Katharina Ganss, Sebastian Hempel, Steffen Wolk, Johanna McChord, Kamal Chowdhury, Philippe Ravassard, Klaus-Peter Knoch, Christian Krautz and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.1field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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  20. Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024
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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 5 institutions in 2 countries.

Hassan MziautMolecular Diabetology, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany; Paul Langerhans Institute Dresden of the Helmholtz Center Munich at the University Hospital and Faculty of Medicine of TU Dresden, Dresden, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.
Georg HennigerDepartment of General, Thoracic, and Vascular Surgery, Faculty of Medicine, TU Dresden, Dresden, Germany.
Katharina GanssMolecular Diabetology, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany; Paul Langerhans Institute Dresden of the Helmholtz Center Munich at the University Hospital and Faculty of Medicine of TU Dresden, Dresden, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.
Sebastian HempelDepartment of General, Thoracic, and Vascular Surgery, Faculty of Medicine, TU Dresden, Dresden, Germany.
Steffen WolkDepartment of General, Thoracic, and Vascular Surgery, Faculty of Medicine, TU Dresden, Dresden, Germany.
Johanna McChordDepartment of General, Thoracic, and Vascular Surgery, Faculty of Medicine, TU Dresden, Dresden, Germany.
Kamal ChowdhuryMax Planck Institute of Biophysical Chemistry, Göttingen, Germany.
Philippe RavassardSorbonne Universités, UPMC Univ Paris 06, INSERM U1127, CNRS UMR 7225, Institut du Cerveau et de la Moelle Épinière, ICM, F-75013, Paris, France.
Klaus-Peter KnochMolecular Diabetology, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany; Paul Langerhans Institute Dresden of the Helmholtz Center Munich at the University Hospital and Faculty of Medicine of TU Dresden, Dresden, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.
Christian KrautzDepartment of Surgery, University of Erlangen, Erlangen, Germany.
Jürgen WeitzDepartment of General, Thoracic, and Vascular Surgery, Faculty of Medicine, TU Dresden, Dresden, Germany.
Robert GrützmannDepartment of Surgery, University of Erlangen, Erlangen, Germany.
Christian PilarskyDepartment of Surgery, University of Erlangen, Erlangen, Germany.
Michele SolimenaMolecular Diabetology, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany; Paul Langerhans Institute Dresden of the Helmholtz Center Munich at the University Hospital and Faculty of Medicine of TU Dresden, Dresden, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. Electronic address: michele.solimena@tu-dresden.de.
Stephan KerstingDepartment of Surgery, University of Erlangen, Erlangen, Germany. Electronic address: stephan.kersting@uk-erlangen.de.
Technische Universität Dresden · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHeinrich Heine University Düsseldorf · DEMax Planck Institute for Biophysical Chemistry · DESorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMicroRNAs (miRNAs) play an integral role in maintaining beta cell function and identity. Deciphering their targets and precise role, however, remains challenging. In this study, we aimed to identify miRNAs and their downstream targets involved in the regeneration of islet beta cells following partial pancreatectomy in mice.

methodsRNA from laser capture microdissected (LCM) islets of partially pancreatectomized and sham-operated mice were profiled with microarrays to identify putative miRNAs implicated in beta cell regeneration. Altered expression of the selected miRNAs, including miR-132, was verified by RT-PCR. Potential targets of miR-132 were selected through bioinformatic data mining. Predicted miR-132 targets were validated for their changed RNA, protein expression levels, and signaling upon miR-132 knockdown and/or overexpression in mouse MIN6 and human EndoC-βH1 insulinoma cells. The ability of miR-132 to foster beta cell proliferation in vivo was further assessed in pancreatectomized miR-132

resultsPartial pancreatectomy significantly increased the number of BrdU

conclusionsThis study provides compelling evidence about the critical role of miR-132 for the regeneration of mouse islet beta cells through the downregulation of its target Pten. Hence, the miR-132/Pten/Akt/Foxo3 signaling pathway may represent a suitable target to enhance beta cell mass.

Indexed as

AnimalsCell ProliferationCells, CulturedCell SurvivalForkhead Box Protein O3HEK293 CellsHumansInsulin-Secreting CellsMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionForkhead Box Protein O3FoxO3 protein, mouseMicroRNAsMIRN132 microRNA, mouseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseApoptosismiR-132PancreatectomyPten/Akt/Foxo3aβ cell regeneration

Identifiers

PMID31918917
PMCPMC6928290
OpenAlexW2989953430

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.