Evidence map›Paper›PMID 32611384›Full record

ArticleBMC nephrology2020

miR-10a overexpression aggravates renal ischemia-reperfusion injury associated with decreased PIK3CA expression.

Dongsheng Xu, Wenjun Li, Tao Zhang, Gang Wang

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 31% 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, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
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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

4 authors at 4 institutions in 1 country.

Dongsheng XuDepartment of Kidney Transplantation, The Second Hospital of Shandong University, Jinan, 250033, China.
Wenjun LiDepartments of Thoracic Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, China.
Tao ZhangDepartment of Cardiac Surgery, Qingdao Fuwai Cardiovascular Hospital, No. 201 Nanjing Road, Shibei District, Qingdao, 266034, China. myzm307@163.com.ORCID 0000-0002-3193-6421
Gang WangDepartment of Cardiac Surgery, Qingdao Fuwai Cardiovascular Hospital, No. 201 Nanjing Road, Shibei District, Qingdao, 266034, China. wg20031998@163.com.
People's Liberation Army 401 Hospital · CNQingdao Center of Resource Chemistry and New Materials · CNQingdao University · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo investigate the effect of miR-10a on renal tissues with ischemia reperfusion (I/R) injury in rats and to explore the underlying mechanisms of the effect of miR-10a on hypoxia-reoxygenation in HK-2 cells.

methodsMiR-10a level was measured in the renal tissues of rats with I/R rats using RT-PCR. In order to research the role of miR-10a in renal tissues, an miR-10 agonist and an miR-10a antagonist were used to treat I/R-injured rats. Levels of serum creatinine and blood urea nitrogen, renal histopathology, and levels of cell apoptosis were analyzed separately in renal tissues from the rats. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway related proteins were measured by Western blotting. In addition, HK-2 cells were cultured in order to study the mechanism of action of miR-10a in the hypoxia-reoxygenation model being studied. Finally, the dual luciferase reporter gene assay was used to confirm that the PI3K p100 catalytic subunit α (PIK3CA) gene was targeted by miR-10a.

resultsAfter renal I/R injury in rats, miR-10a expression increased significantly (p < 0.05). Injection of miR-10a agonist significantly aggravated the renal injury and raised the level of cell apoptosis in the renal tissues of I/R-injured rats (p < 0.05). However, administration of miR-10a antagonist led to obvious improvement of the renal injury, decreased renal cell apoptosis, and inhibited PI3K/Akt pathway activity (p < 0.05). In in vitro experiments, the negative relationship between PIK3CA and miR-10a levels was confirmed. Furthermore, overexpression of miR-10a significantly decreased the proliferation of HK-2 cells, and increased cell apoptosis via up-regulation of the PI3K/Akt pathway (p < 0.05).

conclusionThe aggravation of renal I/R injury by miR-10a was associated with a decrease in the activity of PIK3CA/PI3K/Akt pathway.

Indexed as

AnimalsApoptosisCell LineCell ProliferationClass Ia Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesHumansIn Vitro TechniquesKidneyKidney DiseasesKidney Tubules, ProximalMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsReperfusion InjuryClass Ia Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesMicroRNAsMIRN10 microRNA, humanMIRN10 microRNA, ratPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-aktHypoxia–reoxygenationmiR-10aPIK3CA/PI3K/Akt pathwayRenal ischemia–reperfusion

Identifiers

PMID32611384
PMCPMC7329557
OpenAlexW3040405621

What OpenQuestion holds

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LicenceCC BY
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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.