Evidence map›Paper›PMID 15765100›Full record

ArticleBritish journal of pharmacology2005

Endothelin-1 enhances oxidative stress, cell proliferation and reduces apoptosis in human umbilical vein endothelial cells: role of ETB receptor, NADPH oxidase and caveolin-1.

Feng Dong, Xiaochun Zhang, Loren E Wold, Qun Ren, Zhaojie Zhang, Jun Ren

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.8field-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

78 citing papers in PubMed, 198 citations in OpenAlex.

  1. Article
  2. Article
  3. Endothelin-1/endothelin B receptor signalling mediates Prx1Journal of orthopaedic translation · 2026
    Article
  4. Review
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  12. Article
  13. Molecular pathways that drive diabetic kidney disease.The Journal of clinical investigation · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Frontiers in microbiology · 2022
    Article
  19. Autoantibodies Targeting ATInternational journal of molecular sciences · 2021
    Article
  20. Review

18 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

6 authors at 2 institutions in 1 country.

Feng DongDivision of Pharmaceutical Sciences & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071-3375, USA.
Xiaochun Zhang
Loren E Wold
Qun Ren
Zhaojie Zhang
Jun Ren
University of Wyoming · USUniversity of North Dakota · US

Funding

VENTRICULAR MYOCYTE FUNCTION IN HEALTH AND DISEASEP20RR015640 · NCRR · UNIVERSITY OF WYOMING · PI SKINNER, DONAL C · 2000 to 2010
$15.7M
IGF-1, Oxidative Stress and Cardiovascular AgingR03AG021324 · NIA · UNIVERSITY OF WYOMING · PI REN, JUN · 2002 to 2002
$70k
NCRR NIH HHS P20 RR015640NCRR NIH HHS P20 RR15640NIA NIH HHS R03 AG021324NIA NIH HHS R03 AG21324-01
6 · The paper itself

Abstract

1 Endothelin-1 (ET-1), an endothelium-derived vasoactive peptide, participates in the regulation of endothelial function through mechanisms that are not fully elucidated. This study examined the impact of ET-1 on oxidative stress, apoptosis and cell proliferation in human umbilical vein endothelial cells (HUVEC). HUVECs were challenged for 24 h with ET-1 (10 pM-10 nM) in the absence or presence of the ET(B) receptor antagonist BQ788 (1 microM) or the NADPH oxidase inhibitor apocynin (1 microM). Reactive oxygen species (ROS) were detected using chloromethyl-2',7'-dichlorodihydrofluorescein diacetate. Apoptosis was evaluated with 4',6'-diamidino-2'-phenylindoladihydrochloride staining and by the caspase-3 assay. Cell proliferation was measured by a colorimetric assay. Expression of NADPH oxidase, Akt, pAkt, Bcl-2, Bax, IkappaB, caveolin-1 and eNOS was evaluated by Western blot analysis. 2 ET-1 significantly enhanced ROS generation and cell proliferation following 24-h incubation, both of which were prevented by BQ788 or apocynin, consistent with the ability of ET-1 to directly upregulate NADPH oxidase. ET-1 itself did not affect apoptosis but attenuated homocysteine-induced apoptosis through an ET(B) receptor-mediated mechanism. Western blot analysis indicated that ET-1 alleviated homocysteine (Hcy)-induced apoptosis, likely acting by antagonizing the Hcy-induced decreases in Akt, pAkt, pAkt-to-Akt, Bcl-2-to-Bax ratios and increases in Bax and caveolin-1 expression. Furthermore, ET-1 downregulated expression of caveolin-1 and eNOS, which was attenuated by BQ788 or apocynin. 3 In summary, our results suggest that ET-1 affects oxidative stress, proliferation and apoptosis possibly through ET(B), NADPH oxidase, Akt, Bax and caveolin-1-mediated mechanisms.

Indexed as

ApoptosisCell ProliferationDose-Response Relationship, DrugEndothelin-1Endothelium, VascularHumansNADPH OxidasesOxidative StressReceptor, Endothelin BUmbilical VeinsEndothelin-1NADPH OxidasesReceptor, Endothelin B

Identifiers

PMID15765100
PMCPMC1576147
OpenAlexW2131659594

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.