Evidence map›Paper›PMID 23620807›Full record

ArticlePloS one2013

Toxic effect of silica nanoparticles on endothelial cells through DNA damage response via Chk1-dependent G2/M checkpoint.

Junchao Duan, Yongbo Yu, Yang Li, Yang Yu, Yanbo Li, Xianqing Zhou, Peili Huang, Zhiwei Sun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 189 citations in OpenAlex.

  1. Review
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  13. Experimental study on novel biodegradable Zn-Fe-Si alloys.Journal of biomedical materials research. Part B, Applied biomaterials · 2022
    Article
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  15. CeOToxics · 2022
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  16. Identifying the Molecular Mechanisms and Types of Cell Death Induced byInternational journal of molecular sciences · 2022
    Article
  17. Review
  18. Article
  19. Are Biogenic and Pyrogenic Mesoporous SiOMolecules (Basel, Switzerland) · 2021
    Article
  20. Article

19 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Junchao DuanSchool of Public Health, Capital Medical University, Beijing, PR China.
Yongbo Yu
Yang Li
Yang Yu
Yanbo Li
Xianqing Zhou
Peili Huang
Zhiwei Sun
Capital Medical University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silica nanoparticles have become promising carriers for drug delivery or gene therapy. Endothelial cells could be directly exposed to silica nanoparticles by intravenous administration. However, the underlying toxic effect mechanisms of silica nanoparticles on endothelial cells are still poorly understood. In order to clarify the cytotoxicity of endothelial cells induced by silica nanoparticles and its mechanisms, cellular morphology, cell viability and lactate dehydrogenase (LDH) release were observed in human umbilical vein endothelial cells (HUVECs) as assessing cytotoxicity, resulted in a dose- and time- dependent manner. Silica nanoparticles-induced reactive oxygen species (ROS) generation caused oxidative damage followed by the production of malondialdehyde (MDA) as well as the inhibition of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Both necrosis and apoptosis were increased significantly after 24 h exposure. The mitochondrial membrane potential (MMP) decreased obviously in a dose-dependent manner. The degree of DNA damage including the percentage of tail DNA, tail length and Olive tail moment (OTM) were markedly aggravated. Silica nanoparticles also induced G2/M arrest through the upregulation of Chk1 and the downregulation of Cdc25C, cyclin B1/Cdc2. In summary, our data indicated that the toxic effect mechanisms of silica nanoparticles on endothelial cells was through DNA damage response (DDR) via Chk1-dependent G2/M checkpoint signaling pathway, suggesting that exposure to silica nanoparticles could be a potential hazards for the development of cardiovascular diseases.

Indexed as

DNA DamageApoptosisCheckpoint Kinase 1Comet AssayEndocytosisFlow CytometryG2 Phase Cell Cycle CheckpointsHumansHuman Umbilical Vein Endothelial CellsHydrodynamicsIntracellular SpaceMembrane Potential, MitochondrialNanoparticlesNecrosisOxidative StressParticle SizeCheckpoint Kinase 1CHEK1 protein, humanProtein KinasesReactive Oxygen SpeciesSilicon Dioxide

Identifiers

PMID23620807
PMCPMC3631220
OpenAlexW2060861828

What OpenQuestion holds

Textmetadata
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.