Evidence map›Paper›PMID 24288585›Full record

ArticleOxidative medicine and cellular longevity2013

Effects of endothelial progenitor cell-derived microvesicles on hypoxia/reoxygenation-induced endothelial dysfunction and apoptosis.

Jinju Wang, Shuzhen Chen, Xiaotang Ma, Chuanfang Cheng, Xiang Xiao, Ji Chen, Shiming Liu, Bin Zhao, Yanfang Chen

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
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  4. Review
  5. Review
  6. Review
  7. Article
  8. Extracellular Vesicles in Neurodegenerative Diseases: An Update.International journal of molecular sciences · 2023
    Review
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Review
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  18. Article
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10 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

9 authors at 4 institutions in 2 countries.

Jinju WangDepartment of Pharmacology & Toxicology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH 45435, USA.
Shuzhen Chen
Xiaotang Ma
Chuanfang Cheng
Xiang Xiao
Ji Chen
Shiming Liu
Bin Zhao
Yanfang Chen
Wright State University · USGuangdong Medical College · CNGuangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

Balance of Angiotensin II/Angiotensin (1-1): A Target in Ischemic StrokeR01HL098637 · NHLBI · WRIGHT STATE UNIVERSITY · PI CHEN, YANFANG · 2010 to 2013
$1.4M
NHLBI NIH HHS HL-098637NHLBI NIH HHS R01 HL098637
6 · The paper itself

Abstract

Oxidative stress-induced endothelial dysfunction plays a key role in ischemia/reperfusion injury. Recent evidence indicates that endothelial progenitor cell-derived microvesicles (EPC-MVs) can promote angiogenesis of endothelial cells (ECs). Here, we investigated the potential effects of EPC-MVs on hypoxia/reoxygenation (H/R) injury in human brain microvascular ECs (hb-ECs). MVs were prepared from EPCs cultured in a serum deprivation (SD) medium (starving stress, sEPC-MVs) or SD medium containing tumor necrosis factor- α (TNFα) (apoptotic stress, aEPC-MVs). H/R injury model of hb-ECs was produced by 6 hr hypoxia (1% O2) and 24 hr reoxygenation. The H/R hb-ECs were co-cultured with EPC-MVs. Results showed that (1) H/R hb-ECs were dysfunctional and coupled with increased apoptosis and ROS overproduction; (2) under two different conditions, EPCs displayed remarkable difference in caspase 3 and miR126 expression, which were carried by the corresponsive EPC-MVs; (3) functionally, sEPC-MVs had beneficial effects on H/R hb-ECs, whereas aEPC-MVs had detrimental effects; (4) the diverse effects of sEPC-MVs and aEPC-MVs were associated with the changes in miR126 and eNOS expression and were abolished by PI3K inhibitor. In conclusion, sEPCs-MVs and aEPC-MVs are functionally different on hb-EC apoptosis and dysfunction via their carried RNAs associated with ROS production and PI3K/eNOS/NO pathway.

Indexed as

AnimalsApoptosisBrainCaspase 3Cell-Derived MicroparticlesCell HypoxiaCell SurvivalCulture Media, Serum-FreeEndothelial CellsEndothelium, VascularHumansMiceMicroRNAsMicrovesselsModels, BiologicalNeovascularization, PhysiologicCaspase 3Culture Media, Serum-FreeMicroRNAsMIRN126 microRNA, mouseNitric OxideNitric Oxide Synthase Type IIIOxygenPhosphatidylinositol 3-KinasesReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID24288585
PMCPMC3830832
OpenAlexW2127434261

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.