Evidence map›Paper›PMID 26840039›Full record

ArticleJournal of cellular and molecular medicine2016

High glucose concentration induces endothelial cell proliferation by regulating cyclin-D2-related miR-98.

Xin-Xin Li, Yue-Mei Liu, You-Jie Li, Ning Xie, Yun-Fei Yan, Yong-Liang Chi, Ling Zhou, Shu-Yang Xie, Ping-Yu Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-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

20 citing papers in PubMed, 39 citations in OpenAlex.

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  7. Regulatory Non-coding RNAs in Atherosclerosis.Handbook of experimental pharmacology · 2022
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  14. Article
  15. Comparative Transcriptomics ofJACC. Basic to translational science · 2019
    Article
  16. Sensory Neuropathy Affects Cardiac miRNA Expression Network TargetingInternational journal of molecular sciences · 2019
    Article
  17. 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

9 authors at 4 institutions in 1 country.

Xin-Xin LiDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Yue-Mei LiuDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
You-Jie LiDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Ning XieYantaishan Hospital, Yantai, Shandong, China.
Yun-Fei YanDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Yong-Liang ChiShandong China Traditional Medical Affiliated Hospital, Jinan, China.
Ling ZhouDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Shu-Yang XieDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Ping-Yu WangDepartment of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.
Binzhou Medical University · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNBinzhou University · CNYantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin D2 is involved in the pathology of vascular complications of type 2 diabetes mellitus (T2DM). This study investigated the role of cyclin-D2-regulated miRNAs in endothelial cell proliferation of T2DM. Results showed that higher glucose concentration (4.5 g/l) significantly promoted the proliferation of rat aortic endothelial cells (RAOECs), and significantly increased the expression of cyclin D2 and phosphorylation of retinoblastoma 1 (p-RB1) in RAOECs compared with those under low glucose concentration. The cyclin D2-3' untranslated region is targeted by miR-98, as demonstrated by miRNA analysis software. Western blot also confirmed that cyclin D2 and p-RB1 expression was regulated by miR-98. The results indicated that miR-98 treatment can induce RAOEC apoptosis. The suppression of RAOEC growth by miR-98 might be related to regulation of Bcl-2, Bax and Caspase 9 expression. Furthermore, the expression levels of miR-98 decreased in 4.5 g/l glucose-treated cells compared with those treated by low glucose concentration. Similarly, the expression of miR-98 significantly decreased in aortas of established streptozotocin (STZ)-induced diabetic rat model compared with that in control rats; but cyclin D2 and p-RB1 levels remarkably increased in aortas of STZ-induced diabetic rats compared with those in healthy control rats. In conclusion, this study demonstrated that high glucose concentration induces cyclin D2 up-regulation and miR-98 down-regulation in the RAOECs. By regulating cyclin D2, miR-98 can inhibit human endothelial cell growth, thereby providing novel therapeutic targets for vascular complication of T2DM.

Indexed as

3' Untranslated RegionsAnimalsAortaApoptosisBase SequenceCell ProliferationCyclin D2Diabetes Mellitus, ExperimentalDisease Models, AnimalEndothelial CellsGene Expression RegulationGlucoseMaleMicroRNAsPhosphorylationRats, Sprague-Dawley3' Untranslated RegionsCyclin D2GlucoseMicroRNAsMIRN98 microRNA-98, ratRetinoblastoma Proteincell proliferationcyclin D2gene expressionmiR-98type 2 diabetes

Identifiers

PMID26840039
PMCPMC4882993
OpenAlexW2405250182

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.