Evidence map›Paper›PMID 29070792›Full record

ArticleScientific reports2017

miR-204 is associated with an endocrine phenotype in human pancreatic islets but does not regulate the insulin mRNA through MAFA.

Ilaria Marzinotto, Silvia Pellegrini, Cristina Brigatti, Rita Nano, Raffaella Melzi, Alessia Mercalli, Daniela Liberati, Valeria Sordi, Maurizio Ferrari, Massimo Falconi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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  11. Genetic deletion of miR-204 improves glycemic control despite obesity in db/db mice.Biochemical and biophysical research communications · 2020
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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

14 authors at 2 institutions in 2 countries.

Ilaria MarzinottoDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Silvia PellegriniDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Cristina BrigattiDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Rita NanoDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Raffaella MelziDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Alessia MercalliDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Daniela LiberatiHuman Pathologies Genomic Diagnostics unit, Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy.
Valeria SordiDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Maurizio FerrariHuman Pathologies Genomic Diagnostics unit, Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy.
Massimo FalconiVita-Salute San Raffaele University, Milan, Italy.
Claudio DoglioniVita-Salute San Raffaele University, Milan, Italy.ORCID 0000-0002-4969-5216
Philippe RavassardInstitut du Cerveau et de la Moelle épinière (ICM), Biotechnology & Biotherapy Team, Université Pierre et Marie Curie, Paris, France.
Lorenzo PiemontiDiabetes Research Institute, Division of Immunology, Transplantation and Infectious Disease, IRCCS San Raffaele Scientific Institute, Milan, Italy. piemonti.lorenzo@hsr.it.ORCID 0000-0002-2172-2198
Vito LampasonaHuman Pathologies Genomic Diagnostics unit, Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy. lampasona.vito@hsr.it.ORCID 0000-0001-5162-8445
Vita-Salute San Raffaele University · ITSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-204 has been proposed to modulate insulin expression in human pancreatic islets by regulating the expression of the MAFA transcript, and in turn insulin transcription. We investigated miR-204 expression in pancreatic endocrine tumors (PET), a panel of human tissues, tissues derived from pancreatic islet purification, and in induced pluripotent stem cells (iPSCs) differentiated towards a pancreatic endocrine phenotype by quantitative real time RT-PCR or droplet digital PCR (ddPCR). In addition, we evaluated the effect of miR-204 up- or down-regulation in purified human islets and in the EndoC-βH1 cell line, as an experimental model of human pancreatic β cells. Our results confirm that miR-204 was enriched in insulin producing PET, in β cells within healthy pancreatic islets, and highly expressed in EndoC-βH1 cells. Moreover, in iPSCs miR-204 increased stepwise upon stimulated differentiation to insulin producing cells. However, up- or down-regulation of miR-204 in human islets and in EndoC-βH1 cells resulted in modest and not significant changes of the MAFA and INS mRNAs measured by ddPCR or c-peptide release. Our data confirm the association of miR-204 with a β cell endocrine phenotype in human pancreatic islets, but do not support its direct role in regulating the levels of insulin mRNA through MAFA.

Indexed as

Cell DifferentiationCells, CulturedEndocrine Gland NeoplasmsGene Expression RegulationHumansInduced Pluripotent Stem CellsInsulinIslets of LangerhansMaf Transcription Factors, LargeMicroRNAsPancreatic NeoplasmsPhenotypeRNA, MessengerInsulinMAFA protein, humanMaf Transcription Factors, LargeMicroRNAsMIRN204 microRNA, humanRNA, Messenger

Identifiers

PMID29070792
PMCPMC5656581
OpenAlexW2765370507

What OpenQuestion holds

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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.