Evidence map›Paper›PMID 31187215›Full record

ArticleDiabetologia2019

miR-17-92 and miR-106b-25 clusters regulate beta cell mitotic checkpoint and insulin secretion in mice.

Amitai D Mandelbaum, Sharon Kredo-Russo, Danielle Aronowitz, Nadav Myers, Eran Yanowski, Agnes Klochendler, Avital Swisa, Yuval Dor, Eran Hornstein

Open access · bronzeAbstract read
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In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Amitai D MandelbaumDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Sharon Kredo-RussoDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Danielle AronowitzDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Nadav MyersDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Eran YanowskiDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Agnes KlochendlerDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Avital SwisaDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Yuval DorDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Eran HornsteinDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. eran.hornstein@weizmann.ac.il.
Weizmann Institute of Science · ILHebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisAdult beta cells in the pancreas are the sole source of insulin in the body. Beta cell loss or increased demand for insulin impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. The aim of this study is to test the hypothesis that a family of proto-oncogene microRNAs that includes miR-17-92 and miR-106b-25 clusters regulates beta cell proliferation or function in the adult endocrine pancreas.

methodsTo elucidate the role of miR-17-92 and miR-106b-25 clusters in beta cells, we used a conditional miR-17-92/miR-106b-25 knockout mouse model. We employed metabolic assays in vivo and ex vivo, together with advanced microscopy of pancreatic sections, bioinformatics, mass spectrometry and next generation sequencing, to examine potential targets of miR-17-92/miR-106b-25, by which they might regulate beta cell proliferation and function.

resultsWe demonstrate that miR-17-92/miR-106b-25 regulate the adult beta cell mitotic checkpoint and that miR-17-92/miR-106b-25 deficiency results in reduction in beta cell mass in vivo. Furthermore, we reveal a critical role for miR-17-92/miR-106b-25 in glucose homeostasis and in controlling insulin secretion. We identify protein kinase A as a new relevant molecular pathway downstream of miR-17-92/miR-106b-25 in control of adult beta cell division and glucose homeostasis. CONCLUSIONS/

interpretationThe study contributes to the understanding of proto-oncogene miRNAs in the normal, untransformed endocrine pancreas and illustrates new genetic means for regulation of beta cell mitosis and function by non-coding RNAs. DATA AVAILABILITY: Sequencing data that support the findings of this study have been deposited in GEO with the accession code GSE126516.

Indexed as

AnimalsCells, CulturedFemaleFlow CytometryInsulin-Secreting CellsInsulin SecretionMaleMass SpectrometryMiceMicroRNAsMitosisPancreasMicroRNAsMirn106 microRNA, mouseMIRN17-92 microRNA, mouseBeta cellsCell cycleDiabetesGlucose-stimulated insulin secretionGSISmicroRNAPKAProtein kinase A

Identifiers

PMID31187215
OpenAlexW2950594641

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.