Evidence map›Paper›PMID 26141787›Full record

ArticleDiabetologia2015

The Ia-2β intronic miRNA, miR-153, is a negative regulator of insulin and dopamine secretion through its effect on the Cacna1c gene in mice.

Huanyu Xu, Liron Abuhatzira, Gilberto N Carmona, Suryakiran Vadrevu, Leslie S Satin, Abner L Notkins

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  18. Serum MicroRNA Profiling and Bioinformatics of Patients with Spleen-Deficiency Syndrome.Evidence-based complementary and alternative medicine : eCAM · 2016
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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

6 authors at 2 institutions in 1 country.

Huanyu XuExperimental Medicine Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA.
Liron AbuhatziraExperimental Medicine Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA.
Gilberto N CarmonaExperimental Medicine Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA.
Suryakiran VadrevuBrehm Diabetes Research Center, University of Michigan Medical School, Ann Arbor, MI, USA.
Leslie S SatinBrehm Diabetes Research Center, University of Michigan Medical School, Ann Arbor, MI, USA.
Abner L NotkinsExperimental Medicine Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA. anotkins@dir.nidcr.nih.gov.
National Institutes of Health · USUniversity of Michigan–Ann Arbor · US

Funding

Insulin-Dependent Diabetes MellitusZIADE000423 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI NOTKINS, ABNER L. · 2009 to 2020
$16.9M
METABOLICALLY-COUPLED ION CHANNEL INTERACTIONS IN ISLETSR01DK046409 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SATIN, LESLIE S. · 1994 to 2023
$9.1M
Intramural NIH HHSNIDDK NIH HHS R01 DK046409NIDDK NIH HHS R01DK46409
6 · The paper itself

Abstract

aims/hypothesismiR-153 is an intronic miRNA embedded in the genes that encode IA-2 (also known as PTPRN) and IA-2β (also known as PTPRN2). Islet antigen (IA)-2 and IA-2β are major autoantigens in type 1 diabetes and are important transmembrane proteins in dense core and synaptic vesicles. miR-153 and its host genes are co-regulated in pancreas and brain. The present experiments were initiated to decipher the regulatory network between miR-153 and its host gene Ia-2β (also known as Ptprn2).

methodsInsulin secretion was determined by ELISA. Identification of miRNA targets was assessed using luciferase assays and by quantitative real-time PCR and western blots in vitro and in vivo. Target protector was also employed to evaluate miRNA target function.

resultsFunctional studies revealed that miR-153 mimic suppresses both glucose- and potassium-induced insulin secretion (GSIS and PSIS, respectively), whereas miR-153 inhibitor enhances both GSIS and PSIS. A similar effect on dopamine secretion also was observed. Using miRNA target prediction software, we found that miR-153 is predicted to target the 3'UTR region of the calcium channel gene, Cacna1c. Further studies confirmed that Cacna1c mRNA and protein are downregulated by miR-153 mimics and upregulated by miR-153 inhibitors in insulin-secreting freshly isolated mouse islets, in the insulin-secreting mouse cell line MIN6 and in the dopamine-secreting cell line PC12. CONCLUSIONS/

interpretationmiR-153 is a negative regulator of both insulin and dopamine secretion through its effect on Cacna1c expression, which suggests that IA-2β and miR-153 have opposite functional effects on the secretory pathway.

Indexed as

AnimalsBrainCalcium Channels, L-TypeCell LineDopamineGene Expression RegulationGlucoseInsulinIslets of LangerhansMiceMicroRNAsPancreasReceptor-Like Protein Tyrosine Phosphatases, Class 8CACNA1C protein, mouseCalcium Channels, L-TypeDopamineGlucoseInsulinMicroRNAsMIRN153 microRNA, mousePtprn protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 8Cav1.2IA-2Insulin secretionIntronic miRNAMicroRNAs

Identifiers

PMID26141787
PMCPMC6754265
OpenAlexW825910564

What OpenQuestion holds

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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.