Evidence map›Paper›PMID 24490960›Full record

ArticleJournal of biomedical science2014

Malondialdehyde mediates oxidized LDL-induced coronary toxicity through the Akt-FGF2 pathway via DNA methylation.

Tzu-Ching Yang, Yi-Jie Chen, Shwu-Fen Chang, Chu-Huang Chen, Po-Yuan Chang, Shao-Chun Lu

Abstract read
In one paragraph

Article in Journal of biomedical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Knockdown of lncRNA H19 alleviates ox-LDL-induced HCAECs inflammation and injury by mediating miR-20a-5p/HDAC4 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  7. Review
  8. DNA Methyltransferase 3b Accelerates the Process of Atherosclerosis.Oxidative medicine and cellular longevity · 2022
    Article
  9. Article
  10. The aging endothelium.Vascular biology (Bristol, England) · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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.

Tzu-Ching Yang
Yi-Jie Chen
Shwu-Fen Chang
Chu-Huang Chen
Po-Yuan ChangCardiovascular Center and Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, No, 7, Chung-Shan South Road, Taipei 100, Taiwan. pychang@ntu.edu.tw.
Shao-Chun Lu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidized LDL (oxLDL) is involved in the development of atherosclerotic heart disease through a mechanism that is not fully understood. In this study, we examined the role of malondialdehyde (MDA), an important oxidative stress epitope of oxLDL, in mediating coronary endothelial cytotoxicity.

resultsHuman coronary artery endothelial cells (HCAECs) were treated with oxLDL in the presence or absence of antibody against MDA (anti-MDA) or apoB100 (anti-apoB100). In HCAECs treated with oxLDL (100 μg/ml) alone, DNA synthesis, cell viability, and expression of prosurvival fibroblast growth factor 2 (FGF2) were significantly reduced (P < 0.01 vs phosphate buffered saline-treated cells). These inhibitory effects of oxLDL were significantly attenuated in HCAECs cotreated with anti-MDA (0.15 μg/ml; P < 0.05 vs oxLDL-treated cells), but not in those cotreated with anti-apoB100. When we tested the effects of a panel of signal transduction modifiers on the signal transduction pathways of MDA in oxLDL-treated HCAECs, we found that MDA-induced cytotoxicity was mediated partly through the Akt pathway. Using a reporter gene assay, we identified an oxLDL-response element in the FGF2 promoter that was responsible for the transcriptional repression of FGF2 by oxLDL. The results of bisulfite genomic DNA sequencing showed that in HCAECs treated with oxLDL, the GC-rich promoter of FGF2 was heavily methylated at cytosine residues, whereas cotreatment with anti-MDA markedly reduced oxLDL-induced FGF2 promoter methylation.

conclusionOxLDL disrupts the growth and survival of HCAECs through an MDA-dependent pathway involving methylation of the FGF2 promoter and repression of FGF2 transcription. This novel epigenetic mechanism of oxLDL may underlie its atherogenicity in patients with atherosclerotic cardiovascular disease.

Indexed as

AntibodiesAtherosclerosisCell SurvivalCoronary VesselsDNADNA MethylationEndothelial CellsFibroblast Growth Factor 2HumansLipoproteins, LDLMalondialdehydeOxidative StressProto-Oncogene Proteins c-aktAntibodiesDNAFibroblast Growth Factor 2Lipoproteins, LDLMalondialdehydeoxidized low density lipoproteinProto-Oncogene Proteins c-akt

Identifiers

PMID24490960
PMCPMC3931320

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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.