Evidence map›Paper›PMID 25591776›Full record

ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2015

Ambient fine particulate matter induces apoptosis of endothelial progenitor cells through reactive oxygen species formation.

Yuqi Cui, Xiaoyun Xie, Fengpeng Jia, Jianfeng He, Zhihong Li, Minghuan Fu, Hong Hao, Ying Liu, Jason Z Liu, Peter J Cowan and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Chitosan Nanoparticle-EncapsulatedInternational journal of molecular sciences · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Apoptotic volume decrease (AVD) in AFrontiers in physiology · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

13 authors at 2 institutions in 2 countries.

Yuqi CuiDorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Xiaoyun Xie
Fengpeng Jia
Jianfeng He
Zhihong Li
Minghuan Fu
Hong Hao
Ying Liu
Jason Z Liu
Peter J Cowan
Hua Zhu
Qinghua Sun
Zhenguo Liu
The Ohio State University Wexner Medical Center · USUniversity of Melbourne · AU

Funding

Effects of Oxidized Low-density Lipoprotein on Bone Marrow Stem CellR01HL094650 · NHLBI · OHIO STATE UNIVERSITY · PI LIU, ZHENGUO · 2010 to 2014
$1.9M
Air Pollution on Adiposity and Vascular Dysfunction: White or Brown Matters?R01ES018900 · NIEHS · OHIO STATE UNIVERSITY · PI SUN, QINGHUA · 2011 to 2015
$1.7M
Ambient fine particulate matter and bone marrow stem cellsR01ES026200 · NIEHS · UNIVERSITY OF MISSOURI-COLUMBIA · PI LIU, ZHENGUO · 2016 to 2020
$1.7M
NHLBI NIH HHS NIH R01 HL094650NHLBI NIH HHS R01 HL094650NIEHS NIH HHS R01 ES018900NIEHS NIH HHS R01ES018900NIEHS NIH HHS R01 ES026200
6 · The paper itself

Abstract

BACKGROUND/

aimsBone marrow (BM)-derived endothelial progenitor cells (EPCs) play a critical role in angiogenesis and vascular repair. Some environmental insults, like fine particulate matter (PM) exposure, significantly impair cardiovascular functions. However, the mechanisms for PM-induced adverse effects on cardiovascular system remain largely unknown. The present research was to study the detrimental effects of PM on EPCs and explore the potential mechanisms.

methodsPM was intranasal-distilled into male C57BL/6 mice for one month. Flow cytometry was used to measure the number of EPCs, apoptosis level of circulating EPCs and intracellular reactive oxygen species (ROS) formation. Serum TNF-α and IL-1β were measured using ELISA. To determine the role of PM-induced ROS in EPC apoptosis, PM was co-administrated with the antioxidant N-acetylcysteine (NAC) in wild type mice or used in a triple transgenic mouse line (TG) with overexpression of antioxidant enzyme network (AON) composed of superoxide dismutase (SOD)1, SOD3, and glutathione peroxidase (Gpx-1) with decreased in vivo ROS production.

resultsPM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-α and IL-1β levels, which could be effectively reversed by either NAC treatment or overexpression of AON.

conclusionPM exposure significantly decreased circulating EPCs population due to increased apoptosis via ROS formation in mice.

Indexed as

AcetylcysteineAnimalsApoptosisBone Marrow CellsCells, CulturedEndothelial Progenitor CellsEnzyme-Linked Immunosorbent AssayGlutathione PeroxidaseInterleukin-1betaLungMaleMiceMice, Inbred C57BLParticulate MatterReactive Oxygen SpeciesSuperoxide DismutaseAcetylcysteineGlutathione PeroxidaseInterleukin-1betaParticulate MatterReactive Oxygen SpeciesSod1 protein, mouseSod3 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Tumor Necrosis Factor-alpha

Identifiers

PMID25591776
PMCPMC4309198
OpenAlexW2051195303

What OpenQuestion holds

Textmetadata
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.