Evidence map›Paper›PMID 21126185›Full record

ArticleAntioxidants & redox signaling2011

Adventitia-derived hydrogen peroxide impairs relaxation of the rat carotid artery via smooth muscle cell p38 mitogen-activated protein kinase.

Thomas Cascino, Gabor Csanyi, Imad Al Ghouleh, Augusto C Montezano, Rhian M Touyz, Mounir J Haurani, Patrick J Pagano

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Peripheral vascular remodeling during ischemia.Frontiers in pharmacology · 2022
    Review
  3. Review
  4. Review
  5. NADPH Oxidase Deficiency: A Multisystem Approach.Oxidative medicine and cellular longevity · 2017
    Review
  6. Article
  7. Nox and Inflammation in the Vascular Adventitia.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  8. Article
  9. Article
  10. The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

7 authors at 2 institutions in 2 countries.

Thomas CascinoHypertension and Vascular Research Division, Henry Ford Health System, Detroit, MI, USA.
Gabor Csanyi
Imad Al Ghouleh
Augusto C Montezano
Rhian M Touyz
Mounir J Haurani
Patrick J Pagano
University of Ottawa · CAHenry Ford Health System · US

Funding

Reactive Oxygen Species in Vascular DiseaseR01HL079207 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PAGANO, PATRICK J · 2007 to 2018
$3.4M
HYPERTENSION AND VASCULAR SUPEROXIDE GENERATIONR01HL055425 · NHLBI · HENRY FORD HEALTH SYSTEM · PI PAGANO, PATRICK J · 1998 to 2005
$858k
HYPERTENSION AND VASCULAR SUPEROXIDE GENERATIONR29HL055425 · NHLBI · HENRY FORD HEALTH SYSTEM · PI PAGANO, PATRICK J · 1996 to 1998
–
NHLBI NIH HHS HL079207NHLBI NIH HHS HL55425NHLBI NIH HHS R01 HL079207
6 · The paper itself

Abstract

The role of adventitia-derived reactive oxygen species (ROS) in vascular disease and impaired vascular relaxation is not clear. Based on robust adventitial ROS generation and effects on MAPK involvement in vascular dysfunction, we hypothesized that adventitia-derived ROS hydrogen peroxide (H(2)O(2)) impairs vascular relaxation through activation of medial smooth muscle p38 MAPK. By using a novel in vivo model, the adventitial surface of rat carotid arteries was bathed in situ for 90 min with vehicle, angiotensin II (AngII; 500 nM), AngII+H(2)O(2)-scavenger catalase (3,000 U/ml), AngII+p38 MAPK inhibitor SB203580 (10 μM), or AngII+superoxide dismutase (SOD; 150 U/ml). After these in vivo treatments, ex vivo tone measurements on isolated vessels revealed that periadventitial application of AngII impaired both acetylcholine-induced (endothelium-dependent) and sodium nitroprusside-induced (endothelium-independent) relaxations. In vivo coincubation with catalase or SB203580 significantly improved, but SOD exacerbated AngII-induced impairment of in vitro endothelium-dependent and -independent vascular relaxations. Western blots of vascular media, separated from the adventitia, demonstrated increased medial p38 MAPK activation and decreased medial phosphatase SHP-2 activity in AngII-treated vessels. These effects were reversed by in vivo periadventitial addition of catalase. These findings provide the first evidence that adventitia-derived H(2)O(2) participates in vascular dysfunction through p38 MAPK activation and SHP-2 inhibition.

Indexed as

Muscle RelaxationAngiotensin IIAnimalsCarotid ArteriesCatalaseConnective TissueDisease Models, AnimalHydrogen PeroxideImidazolesMaleMyocytes, Smooth MuscleMyographyp38 Mitogen-Activated Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PyridinesRatsAngiotensin IICatalaseHydrogen PeroxideImidazolesp38 Mitogen-Activated Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PyridinesSB 203580Superoxide Dismutase

Identifiers

PMID21126185
PMCPMC3151421
OpenAlexW2046300908

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.