Evidence map›Paper›PMID 29290993›Full record

ArticleOncotarget2017

MicroRNA-34c acts as a bidirectional switch in the maturation of insulin-producing cells derived from mesenchymal stem cells.

Chunyu Bai, Yuhua Gao, Xiangyang Zhang, Wancai Yang, Weijun Guan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
1.0field-weighted citation impact, top 27% 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, 27 citations in OpenAlex.

  1. Pooled it
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  6. miRNAs as Biomarkers in Diabetes: Moving towards Precision Medicine.International journal of molecular sciences · 2022
    Review
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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

5 authors at 4 institutions in 2 countries.

Chunyu BaiKey Laboratory of Precision Oncology of Shandong Higher Education, Institute of Precision Medicine, Jining Medical University, Jining, 272067, PR China.
Yuhua GaoCollege of Basic Medicine, Jining Medical University, Jining, 272067, PR China.
Xiangyang ZhangCollege of Basic Medicine, Jining Medical University, Jining, 272067, PR China.
Wancai YangKey Laboratory of Precision Oncology of Shandong Higher Education, Institute of Precision Medicine, Jining Medical University, Jining, 272067, PR China.
Weijun GuanInstitute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193, PR China.
Institute of Animal Sciences · CNChinese Academy of Agricultural Sciences · CNJining Medical University · CNUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miRNAs regulate insulin secretion, pancreatic development, and beta-cell differentiation. However, their function in the differentiation of IPCs from MSCs is poorly understood. In this study, to screen for miRNAs and their targets that function during the formation of IPCs from MSCs, we examined the miRNA expression profiles of MSCs and IPCs using RNA-seq and qPCR to confirm the above results. We found that miR-34c exhibited transient upregulation at an early stage of the formation of IPCs derived from MSCs. Next, we analyzed the biological function of miR-34c by predicting its targets using bioinformatic tools. Combining our data with those from previous reports, we found that miR-34c and its targets play an important role in the formation of IPCs. Therefore, we overexpressed miR-34c and expressed small interfering RNAs of its targets in MSCs to investigate their functions in IPC formation. We found that miR-34c acts as a bidirectional switch in the formation of IPCs derived from MSCs by regulating the expression of targets to affect insulin synthesis and secretion. miR-34c was shown to downregulate its targets, including PDE7B, PDGFRA, and MAP2K1, to increase proinsulin synthesis, but when miR-34c continually dysregulated such expression, it suppressed the expression of other targets, namely ACSL4 and SAR1A, weakening insulin secretion in IPCs. These results suggest that endogenous miRNAs involved in the formation of IPCs from stem cells should be considered in the development of effective cell transplant therapy for diabetes.

Indexed as

differentiationinsulin-producing cellinsulin secretionmesenchymal stem cellsmiR-34c

Identifiers

PMID29290993
PMCPMC5739778
OpenAlexW2765709371

What OpenQuestion holds

Textmetadata
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.