Evidence map›Paper›PMID 31532760›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Inhibition of microRNA-141-3p Reduces Hypoxia-Induced Apoptosis in H9c2 Rat Cardiomyocytes by Activating the RP105-Dependent PI3K/AKT Signaling Pathway.

Qiaoji Qin, Liqiang Cui, Zhenggang Zhou, Zhirong Zhang, Yini Wang, Changyong Zhou

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 31 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

6 authors at 2 institutions in 1 country.

Qiaoji QinDepartment of Emergency Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Liqiang CuiDepartment of Anesthesiology, Qingdao Chengyang People's Hospital, Qingdao, Shandong, China (mainland).
Zhenggang ZhouDepartment of Spine Surgery, Qingdao Chengyang People's Hospital, Qingdao, Shandong, China (mainland).
Zhirong ZhangDepartment of Emergency Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Yini WangDepartment of Emergency Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Changyong ZhouDepartment of Emergency Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Oxidative stress in myocardial ischemia results in cardiomyocyte apoptosis. The expression of microRNA-141-3p (miR-141-3p) and the 105 kD toll-like receptor protein (TLR), RP105, have been identified in cardiomyocytes in vitro. This study aimed to investigate the effects of hypoxia in H9c2 rat cardiomyoblasts with and without the inhibition of miR-141-3p and to investigate the expression of RP105 and the PI3K/AKT signaling pathway. MATERIAL AND METHODS H9c2 rat cardiomyoblasts were cultured in conditions of hypoxia and treated with a specific miR-141-3p-inhibitor. RP105 short-interfering RNA (siRNA) was constructed, and LY294002 was used to inhibit the PI3KA/AKT pathway. The fluorescent probe, dihydroethidium (DHE), was used to detect reactive oxygen species (ROS). Flow cytometry evaluated ROS and apoptosis. Quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot studied the expression of the PI3K/AKT pathway genes and proteins. Bioinformatics and dual-luciferase reporter assays were used to identify the targets for miR-141-3p. RESULTS A predictive TargetScan algorithm showed that the RP105 gene was a potential target of miR-141-3p. Expression of miR-141-3p was significantly increased in hypoxic H9c2 cells, and inhibition of miR-141-3p increased cell viability and reduced apoptosis. Also, miR-141-3p was shown to target 3'-UTR of RP105. Down-regulation of RP105 associated with hypoxia and its downstream PI3K/AKT pathway were significantly increased following miR-141-3p inhibition. The protective effect of miR-141-3p inhibition in hypoxic H9c2 cells was abolished by the absence of RP105 and inhibition of PI3K/AKT. CONCLUSIONS Inhibition of miR-141-3p reduced hypoxia-induced apoptosis in H9c2 cardiomyocytes in vitro by activating the RP105-dependent PI3K/AKT signaling pathway.

Indexed as

ApoptosisSignal TransductionAnimalsAntigens, CDBase SequenceCell HypoxiaCell LineMicroRNAsMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsUp-RegulationAntigens, CDCd180 protein, ratMicroRNAsMirn141 microRNA, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31532760
PMCPMC6765341
OpenAlexW2974693203

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.