Evidence map›Paper›PMID 25256620›Full record

ArticleJournal of cellular and molecular medicine2014

Cell membrane damage is involved in the impaired survival of bone marrow stem cells by oxidized low-density lipoprotein.

Xin Li, Yuan Xiao, Yuqi Cui, Tao Tan, Chandrakala A Narasimhulu, Hong Hao, Lingjuan Liu, Jia Zhang, Guanglong He, Catherine M Verfaillie and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Oxidative Stress, Endothelial Dysfunction, andAntioxidants & redox signaling · 2024
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  11. Orally administered gadolinium orthovanadate GdVOWiener medizinische Wochenschrift (1946) · 2020
    Article
  12. Article
  13. Article
  14. Mesenchymal Stem Cells Alleviate Acute Lung Injury and Inflammatory Responses Induced by Paraquat Poisoning.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  15. Article
  16. 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

15 authors at 4 institutions in 3 countries.

Xin LiXiangya Hospital of Central South University, Changsha, Hunan, China; Davis Heart & Lung Research Institute and Division of Cardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Yuan Xiao
Yuqi Cui
Tao Tan
Chandrakala A Narasimhulu
Hong Hao
Lingjuan Liu
Jia Zhang
Guanglong He
Catherine M Verfaillie
Minxiang Lei
Sampath Parthasarathy
Jianjie Ma
Hua Zhu
Zhenguo Liu
The Ohio State University Wexner Medical Center · USCentral South University · CNUniversity of Central Florida · USKU Leuven · BE

Funding

Modulation of MG53 Function in Cardiac Membrane RepairR01HL069000 · NHLBI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MA, JIANJIE · 2002 to 2016
$5.3M
MG53-Mediated Membrane Repair in Muscle Physiology and DiseaseR01AR061385 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LIN, PEI-HUI · 2011 to 2020
$3.8M
Effects of Oxidized Low-density Lipoprotein on Bone Marrow Stem CellR01HL094650 · NHLBI · OHIO STATE UNIVERSITY · PI LIU, ZHENGUO · 2010 to 2014
$1.9M
NHLBI NIH HHS NIH R01 HL094650NHLBI NIH HHS R01 HL069000NHLBI NIH HHS R01 HL094650NIAMS NIH HHS R01 AR061385
6 · The paper itself

Abstract

Cell therapy with bone marrow stem cells (BMSCs) remains a viable option for tissue repair and regeneration. A major challenge for cell therapy is the limited cell survival after implantation. This study was to investigate the effect of oxidized low-density lipoprotein (ox-LDL, naturally present in human blood) on BMSC injury and the effect of MG53, a tissue repair protein, for the improvement of stem cell survival. Rat bone marrow multipotent adult progenitor cells (MAPCs) were treated with ox-LDL, which caused significant cell death as reflected by the increased LDH release to the media. Exposure of MAPCs to ox-LDL led to entry of fluorescent dye FM1-43 measured under confocal microscope, suggesting damage to the plasma membrane. Ox-LDL also generated reactive oxygen species (ROS) as measured with electron paramagnetic resonance spectroscopy. While antioxidant N-acetylcysteine completely blocked ROS production from ox-LDL, it failed to prevent ox-LDL-induced cell death. When MAPCs were treated with the recombinant human MG53 protein (rhMG53) ox-LDL induced LDH release and FM1-43 dye entry were significantly reduced. In the presence of rhMG53, the MAPCs showed enhanced cell survival and proliferation. Our data suggest that membrane damage induced by ox-LDL contributed to the impaired survival of MAPCs. rhMG53 treatment protected MAPCs against membrane damage and enhanced their survival which might represent a novel means for improving efficacy for stem cell-based therapy for treatment of diseases, especially in setting of hyperlipidemia.

Indexed as

AcetylcysteineAnimalsBone Marrow CellsCarrier ProteinsCell MembraneCell ProliferationCells, CulturedCell SurvivalDose-Response Relationship, DrugFluorescent DyesFree Radical ScavengersHumansLipoproteins, LDLMicroscopy, ConfocalMultipotent Stem CellsPyridinium CompoundsAcetylcysteineCarrier ProteinsFluorescent DyesFM1 43Free Radical ScavengersLipoproteins, LDLoxidized low density lipoproteinPyridinium CompoundsQuaternary Ammonium CompoundsReactive Oxygen SpeciesRecombinant ProteinsTRIM72 protein, humanTripartite Motif Proteinscell survivalmembrane damagemesenchymal stem cellsMG53ox-LDL

Identifiers

PMID25256620
PMCPMC4302650
OpenAlexW2031517346

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.