Evidence map›Paper›PMID 25985365›Full record

ArticleNature medicine2015

The microRNA-200 family regulates pancreatic beta cell survival in type 2 diabetes.

Bengt-Frederik Belgardt, Kashan Ahmed, Martina Spranger, Mathieu Latreille, Remy Denzler, Nadiia Kondratiuk, Ferdinand von Meyenn, Felipe Nunez Villena, Karolin Herrmanns, Domenico Bosco and 4 more

Abstract read
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In one paragraph

Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

158 citing papers in PubMed, 1 synthesis or guideline pooled it.

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98 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Bengt-Frederik Belgardt1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Kashan Ahmed1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Martina Spranger1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Mathieu Latreille1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Remy Denzler1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Nadiia Kondratiuk1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Ferdinand von Meyenn1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.ORCID 0000000199203075
Felipe Nunez Villena1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Karolin Herrmanns1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.
Domenico BoscoCell Isolation and Transplantation Center, Department of Surgery, University Hospitals and University of Geneva, Geneva, Switzerland.
Julie Kerr-ConteUniversité de Lille 2, INSERM, European Genomic Institute for Diabetes, Lille Cedex, France.
Francois PattouUniversité de Lille 2, INSERM, European Genomic Institute for Diabetes, Lille Cedex, France.
Thomas RülickeInstitute of Laboratory Animal Science, University of Veterinary Medicine Vienna, Vienna, Austria.
Markus Stoffel1] Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. [2] Competence Center for Systems Physiology and Metabolic Disease, Swiss Federal Institute of Technology, Zurich, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic beta cell death is a hallmark of type 1 (T1D) and type 2 (T2D) diabetes, but the molecular mechanisms underlying this aspect of diabetic pathology are poorly understood. Here we report that expression of the microRNA (miR)-200 family is strongly induced in islets of diabetic mice and that beta cell-specific overexpression of miR-200 in mice is sufficient to induce beta cell apoptosis and lethal T2D. Conversely, mir-200 ablation in mice reduces beta cell apoptosis and ameliorates T2D. We show that miR-200 negatively regulates a conserved anti-apoptotic and stress-resistance network that includes the essential beta cell chaperone Dnajc3 (also known as p58IPK) and the caspase inhibitor Xiap. We also observed that mir-200 dosage positively controls activation of the tumor suppressor Trp53 and thereby creates a pro-apoptotic gene-expression signature found in islets of diabetic mice. Consequently, miR-200-induced T2D is suppressed by interfering with the signaling of Trp53 and Bax, a proapoptotic member of the B cell lymphoma 2 protein family. Our results reveal a crucial role for the miR-200 family in beta cell survival and the pathophysiology of diabetes.

Indexed as

AnimalsApoptosisCell SurvivalDiabetes Mellitus, Type 2Gene Expression RegulationHSP40 Heat-Shock ProteinsHumansInsulinInsulin-Secreting CellsMiceMice, Inbred NODMicroRNAsSignal TransductionX-Linked Inhibitor of Apoptosis ProteinDnajc3 protein, mouseHSP40 Heat-Shock ProteinsInsulinMicroRNAsMirn200 microRNA, mouseX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID25985365

What OpenQuestion holds

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Registered trials

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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.