Evidence map›Paper›PMID 28713945›Full record

ArticleMolecular medicine reports2017

miR‑433 protects pancreatic β cell growth in high‑glucose conditions.

Min Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Min WangDepartment of Endocrinology, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China.
Hunan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic β cell dysfunction is a key characteristic in the pathogenesis of diabetes mellitus (DM). MicroRNAs (miRNAs) have been identified to serve a role in DM pathogenesis, but how specific miRNAs regulate glucose‑stimulated β cell functions remain unclear. The present study aimed to explore the effects of miR‑433 on cell growth under high‑glucose culture conditions and to determine the possible mechanisms involved. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis was performed to detect the expression levels of miRNAs in Min‑6 pancreatic β cells cultured in high‑glucose medium, which revealed that miR‑433 was significantly downregulated. Results from in vitro Cell Counting Kit‑8, colony formation and flow cytometry analyses indicated that overexpression of miR‑433 may enhance cell viability and proliferation by promoting cell cycle progression and suppressing apoptosis. Furthermore, bioinformatics prediction and luciferase analysis demonstrated that miR‑433 was able to inhibit the expression of cyclooxygenase 2 (COX2) through targeting its 3'‑UTR. Moreover, knockdown of COX2 expression alleviated the inhibition of cell growth induced by high glucose, similar to overexpression of miR‑433. In conclusion, the present results suggested that miR‑433 may protect pancreatic β cells cultured in high glucose, which suggests that miR‑433 may have beneficial effects in preventing and treating DM.

Indexed as

Cell Proliferation3' Untranslated RegionsAnimalsApoptosisCell Cycle CheckpointsCyclooxygenase 2Gene Expression RegulationGlucoseHEK293 CellsHumansInsulin-Secreting CellsMiceMicroRNAsUp-Regulation3' Untranslated RegionsCyclooxygenase 2GlucoseMicroRNAsMirn433 microRNA, mousePtgs2 protein, mouse

Identifiers

PMID28713945
PMCPMC5548008
OpenAlexW2724161056

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.