Evidence map›Paper›PMID 30186503›Full record

ArticleExperimental and therapeutic medicine2018

miR-192 is upregulated in T1DM, regulates pancreatic β-cell development and inhibits insulin secretion through suppressing GLP-1 expression.

Wen Pan, Yanan Zhang, Chun Zeng, Fen Xu, Jinhua Yan, Jianping Weng

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 33% 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, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  11. Role and Mechanism of Gut Microbiota in Human Disease.Frontiers in cellular and infection microbiology · 2021
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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.

Wen PanDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Yanan ZhangDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Chun ZengDepartment of Emergency, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Fen XuDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Jinhua YanDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Jianping WengDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRs) post-translationally regulate gene expression by specifically binding to the mRNA of their target genes. The aim of the present study was to determine the effect of miR-192 on pancreatic β-cell development. The serum levels of miR-192 in type 1 diabetes mellitus (T1DM) and streptozotocin-induced rats were determined, and were revealed to be elevated compared with those in healthy patients and normal rats, respectively. Western blot and reverse transcription-quantitative polymerase chain reaction analysis indicated that miR-192 suppressed the expression of glucagon-like peptide-1 (GLP-1), a potent insulin secretagogue. Ectopic expression of miR-192 inhibited cell proliferation and promoted apoptosis of NIT-1 cells, while miR-192 inhibitor had the opposite effect. Collectively, the present results revealed that miR-192 was elevated in T1DM, and is implicated in pancreatic β-cell development through regulation of cell proliferation and apoptosis, thereby suppressing insulin secretion. Furthermore, miR-192 suppressed GLP-1 expression, thereby further promoting T1DM. The present study suggested that miR-192 is a novel molecular target for the management or prevention of T1DM.

Indexed as

glucagon-like peptide-1insulinmicroRNA-192proliferationtype 1 diabetes mellitus

Identifiers

PMID30186503
PMCPMC6122452
OpenAlexW2884405257

What OpenQuestion holds

Textmetadata
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.