Evidence map›Paper›PMID 24454982›Full record

ArticleOxidative medicine and cellular longevity2013

Differential microRNA profiling in a cellular hypoxia reoxygenation model upon posthypoxic propofol treatment reveals alterations in autophagy signaling network.

Zhuo Chen, Zhe Hu, Zhiqi Lu, Shuyun Cai, Xiaoxia Gu, Haixia Zhuang, Zhihua Ruan, Zhengyuan Xia, Michael G Irwin, Du Feng and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

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  12. Sodium Tanshinone IIA Sulfonate Prevents Radiation-Induced Toxicity in H9c2 Cardiomyocytes.Evidence-based complementary and alternative medicine : eCAM · 2017
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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

11 authors at 3 institutions in 2 countries.

Zhuo ChenDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Zhe HuDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Zhiqi LuDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Shuyun CaiDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Xiaoxia GuDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Haixia ZhuangDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Zhihua RuanDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Zhengyuan XiaAnesthesiology Research Laboratory, Department of Anesthesiology, University of Hong Kong, Hong Kong.
Michael G IrwinAnesthesiology Research Laboratory, Department of Anesthesiology, University of Hong Kong, Hong Kong.
Du FengKey Laboratory of Age-Associated Cardiac-Cerebral Vascular Disease of Guangdong Province, Department of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Liangqing ZhangDepartment of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
Guangdong Medical College · CNChinese University of Hong Kong · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies indicate that propofol may protect cells via suppressing autophagic cell death caused by excessive reactive oxygen species induced by hypoxia reoxygenation (H/R). It is established that gene expression patterns including autophagy-related genes changed significantly during the process of H/R in the presence or absence of propofol posthypoxia treatment (P-PostH). The reasons for such differences, however, remain largely unknown. MicroRNAs provide a novel mechanism for gene regulation. In the present study, we systematically analyzed the alterations in microRNA expression using human umbilical vein endothelial cells (HUVECs) subjected to H/R in the presence or absence of posthypoxic propofol treatment. Genome-wide profiling of microRNAs was then conducted using microRNA microarray. Fourteen miRNAs are differentially expressed and six of them were validated by the quantitative real-time PCR (Q-PCR) of which three were substantially increased, whereas one was decreased. To gain an unbiased global perspective on subsequent regulation by altered miRNAs, predicted targets of ten miRNAs were analyzed using the Gene Ontology (GO) analysis to build signaling networks. Interestingly, six of the identified microRNAs are known to target autophagy-related genes. In conclusion, our results revealed that different miRNA expression patterns are induced by propofol posthypoxia treatment in H/R and the alterations in miRNA expression patterns are implicated in regulating distinctive autophagy-related gene expression.

Indexed as

Gene Expression ProfilingModels, BiologicalAutophagyCell HypoxiaCell SurvivalGene Expression RegulationGene Regulatory NetworksHumansHuman Umbilical Vein Endothelial CellsMicroRNAsOligonucleotide Array Sequence AnalysisOxygenPropofolReproducibility of ResultsSignal TransductionMicroRNAsOxygenPropofol

Identifiers

PMID24454982
PMCPMC3885199
OpenAlexW2099540233

What OpenQuestion holds

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LicenceCC BY
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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.