Evidence map›Paper›PMID 30096614›Full record

ArticleRedox biology2018

Decreases in GSH:GSSG activate vascular endothelial growth factor receptor 2 (VEGFR2) in human aortic endothelial cells.

Priya K Prasai, Bandana Shrestha, A Wayne Orr, Christopher B Pattillo

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  5. Review
  6. DietaryAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2022
    Article
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  11. Review
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  15. Article
  16. Mechanoresponse of stem cells for vascular repair.World journal of stem cells · 2019
    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

4 authors at 1 institution in 1 country.

Priya K PrasaiDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Bandana ShresthaDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
A Wayne OrrDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA; Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA; Department of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Christopher B PattilloDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA. Electronic address: cpatt7@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · US

Funding

Stress Exacerbates Myocardial Ischemic Injury by Blocking Estrogen's Antidoxidant Protection in the Female HeartP20GM121307 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI Vesna Tesic · 2018 to 2026
$23.6M
Nck Adaptor Proteins in Atherogenic Endothelial ActivationR01HL133497 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2016 to 2024
$3.8M
Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
NHLBI NIH HHS R01 HL098435NHLBI NIH HHS R01 HL133497NIGMS NIH HHS P20 GM121307
6 · The paper itself

Abstract

The angiogenic capacity of local tissue critically regulates the response to ischemic injury. Elevated reactive oxygen species production, commonly associated with ischemic injury, has been shown to promote phosphorylation of the vascular endothelial growth factor receptor 2 (VEGFR2), a critical regulator of angiogenesis. Previous data from our lab demonstrated that diminished levels of the antioxidant glutathione positively augment ischemic angiogenesis. Here, we sought to determine the relationship between glutathione levels and oxidative stress in VEGFR2 signaling. We reveal that decreasing the ratio of GSH to GSSG with diamide leads to enhanced protein S-glutathionylation, increased reactive oxygen species (ROS) production, and enhanced VEGFR2 activation. However, increasing ROS alone was insufficient in activating VEGFR2, while ROS enhanced VEGF-stimulated VEGFR2 activation at supraphysiological levels. We also found that inhibiting glutathione reductase activity is sufficient to increase VEGFR2 activation and sensitizes cells to ROS-dependent VEGFR2 activation. Taken together, these data suggest that regulation of the cellular GSH:GSSG ratio critically regulates VEGFR2 activation. This work represents an important first step in separating thiol mediated signaling events from ROS dependent signaling.

Indexed as

Oxidative StressAortaCell LineEndothelial CellsGlutathioneGlutathione DisulfideHumansOxidation-ReductionVascular Endothelial Growth Factor Receptor-2GlutathioneGlutathione DisulfideKDR protein, humanVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID30096614
PMCPMC6086407
OpenAlexW2883164193

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.