Evidence map›Paper›PMID 25360679›Full record

ArticlePloS one2014

Hepatocyte growth factor modification enhances the anti-arrhythmic properties of human bone marrow-derived mesenchymal stem cells.

Jian Zhang, Lin-Lin Wang, Wei Du, Yi-Chao Yu, Wei-Zhu Ju, Yi-Long Man, Xiao-Rong Li, Yan Chen, Zi-Dun Wang, Wei-Juan Gu and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. 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

14 authors at 3 institutions in 1 country.

Jian ZhangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Lin-Lin WangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Wei DuDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yi-Chao YuDepartment of Cardiology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Wei-Zhu JuDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yi-Long ManDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Xiao-Rong LiDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yan ChenDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Zi-Dun WangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Wei-Juan GuDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Feng-Xiang ZhangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Hua WangDepartment of Experimental Hematology, Beijing Institute of Radiation Medicine, Beijing, People's Republic of China.
Chu-Tse WuDepartment of Experimental Hematology, Beijing Institute of Radiation Medicine, Beijing, People's Republic of China.
Ke-Jiang CaoDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Nanjing Medical University · CNJiangsu Province Hospital · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsChronic myocardial infarction (MI) results in the formation of arrhythmogenic substrates, causing lethal ventricular arrhythmia (VA). We aimed to determine whether mesenchymal stem cells (MSCs) carrying a hepatocyte growth factor (HGF) gene modification (HGF-MSCs) decrease the levels of arrhythmogenic substrates and reduce the susceptibility to developing VA compared with unmodified MSCs and PBS in a swine infarction model.

methodsThe left descending anterior artery was balloon-occluded to establish an MI model. Four weeks later, the randomly grouped pigs were administered MSCs, PBS or HGF-MSCs via thoracotomy. After an additional four weeks, dynamic electrocardiography was performed to assess heart rate variability, and programmed electrical stimulation was conducted to evaluate the risk for VA. Then, the pigs were euthanized for morphometric, immunofluorescence and western blot analyses.

resultsThe HGF-MSC group displayed the highest vessel density and Cx43 expression levels, and the lowest levels of apoptosis, and tyrosine hydroxylase (TH) and growth associated protein 43 (GAP43) expression. Moreover, the HGF-MSC group exhibited a decrease in the number of sympathetic nerve fibers, substantial decreases in the low frequency and the low-/high- frequency ratio and increases in the root mean square of successive differences (rMSSD) and the percentage of successive normal sinus R-R intervals longer than 50 ms (pNN50), compared with the other two groups. Finally, the HGF-MSC group displayed the lowest susceptibility to developing VA.

conclusionHGF-MSCs displayed potent antiarrhythmic effects, reducing the risk for VA.

Indexed as

Mesenchymal Stem Cell TransplantationAnimalsApoptosisArrhythmias, CardiacAutonomic Nervous SystemBone Marrow CellsCell SurvivalElectric StimulationGene Expression RegulationHeart VentriclesHepatocyte Growth FactorHumansMaleMesenchymal Stem CellsMyocardial InfarctionNeovascularization, PhysiologicHepatocyte Growth Factor

Identifiers

PMID25360679
PMCPMC4216066
OpenAlexW2092469307

What OpenQuestion holds

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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.