Evidence map›Paper›PMID 27602317›Full record

ArticleCell journal2016

Development of Insulin Resistance through Induction of miRNA-135 in C2C12 Cells.

Maryam Honardoost, Ehsan Arefian, Masoud Soleimani, Sara Soudi, Mohammad Reza Sarookhani

Open access · greenAbstract read
In one paragraph

Article in Cell journal, 2016. 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
1.2field-weighted citation impact, top 23% 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, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. The Destiny of Glucose from a MicroRNA Perspective.Frontiers in endocrinology · 2018
    Review
  7. Article
  8. Article
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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 3 institutions in 1 country.

Maryam HonardoostDepartment of Molecular Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran; Stem Cell Technology Research Center, Tehran, Iran.
Ehsan ArefianDepartment of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Masoud SoleimaniDepartment of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Sara SoudiDepartment of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Mohammad Reza SarookhaniDepartment of Molecular Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran.
Tarbiat Modares University · IRQazvin University of Medical Sciences · IRUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMicro-RNAs (miRNAs) are a class of posttranscriptional regulators that play crucial roles in various biological processes. Emerging evidence suggests a direct link between miRNAs and development of several diseases including type 2 diabetes (T2D). In this study, we aimed to investigate the effect of predicted miRNA and target genes on insulin resistance. MATERIALS AND

methodsThis experimental study was conducted on the C2C12 cell line. Using bioinformatics tools miRNA-135 and two respective target genes-insulin receptor (Insr) and vesicle associated membrane protein 2 (Vamp2)were selected as potential factors involved in insulin resistance process. Levels of glucose uptake miRNA expression and respective gene targets were determined after cell transfaction by miR-135.

resultsIt was determined that Insr gene expression was significantly down-regulated in miR-135 transfected C2C12 cell line (P≤0.05). Interestingly; these transfected cells have shown a significant difference in glucose uptake incomparision the positive control cells, while it was similar to the insulin resistant cell line (P≤0.05). In contrast, no significant alteration of Vamp2 gene expression was observed.

conclusionOur data indicated no change on the Vamp2 expression level after miRNA transfection, while expression level of Insr was reduced and miR-135 expression was contrarily increased leading to poor stimulation of glucose uptake through insulin, and development of insulin resistance phenotype in C2C12 cell line.

Indexed as

C2C12Insulin ReceptorInsulin ResistanceMiR-135

Identifiers

PMID27602317
PMCPMC5011323
OpenAlexW2520347050

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.