Evidence map›Paper›PMID 26438597›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2016

Matrix Metalloproteinase 1 Causes Vasoconstriction and Enhances Vessel Reactivity to Angiotensin II via Protease-Activated Receptor 1.

William H Nugent, Nikita Mishra, Jerome F Strauss, Scott W Walsh

Open access · bronzeAbstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  7. Article
  8. The Effects of Low Concentrations of Pravastatin on Placental Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
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  16. Review
  17. Article
  18. Article
  19. Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  20. 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.

William H NugentDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, VA, USA.
Nikita MishraDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, VA, USA Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, VA, USA.
Jerome F StraussDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, VA, USA.
Scott W WalshDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, VA, USA Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, VA, USA Scott.Walsh@vcuhealth.org.
Virginia Commonwealth University Medical Center · US

Funding

Oxidant Stress Mechanisms in PreeclampsiaR01HL069851 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WALSH, SCOTT W · 2003 to 2013
$2.7M
NHLBI NIH HHS R01 HL069851
6 · The paper itself

Abstract

Matrix metalloproteinase 1 (MMP-1) is an activator of protease-activated receptor 1 (PAR-1), which is known to mediate the release of endothelin 1 (ET-1) in endothelial cells and activate the RhoA kinase (ROCK) pathway. Recently, we reported increased serum and vascular MMP-1 in women with preeclampsia and hypothesized that the action of MMP-1 on PAR-1 might have vasoconstrictive effects. Resistance-sized omental arteries obtained from normal pregnant women were mounted on a myograph system and perfused with MMP-1 in a dose range of 0.025 to 25 ng/mL or with angiotensin II (Ang II) in a dose range of 0.001 to 10 µmol/L in the presence of intraluminal MMP-1 (2.5 ng/mL) perfusion. Angiotensin II dose response was also performed with omental arteries from women with preeclampsia. Matrix metalloproteinase 1 caused dose-dependent vasoconstriction in endothelium-intact, but not in endothelium-denuded, vessels from normal pregnant women, which was blocked by inhibitors of PAR-1 and ET-1 type A receptor blocker. Intraluminal perfusion with a constant amount of MMP-1 enhanced vessel reactivity to Ang II, which was blocked by inhibitors of PAR-1, ROCK, and ET-1. Enhanced vascular reactivity to Ang II was observed in endothelium-intact, but not in endothelium-denuded, arteries of women with preeclampsia. Inhibitors of PAR-1, ROCK, and ET-1 blocked enhanced vascular reactivity to Ang II in endothelium-intact preeclamptic arteries. These data demonstrate that MMP-1 has potent vasoconstrictor effects and the ability to enhance vascular reactivity to vasoconstrictor hormones, which are mediated by an endothelial PAR-1, ROCK, and ET-1 pathway. Increased circulating levels of MMP-1 and its increased expression in systemic vessels of women with preeclampsia may contribute to the development of maternal hypertension.

Indexed as

AdultAngiotensin IIDose-Response Relationship, DrugDrug SynergismFemaleHumansMatrix Metalloproteinase 1OmentumOrgan Culture TechniquesPlatelet Aggregation InhibitorsPre-EclampsiaPregnancyPyrrolesQuinazolinesReceptor, PAR-1VasoconstrictionAngiotensin IIMatrix Metalloproteinase 1N3-cyclopropyl-7-((4-(1-methylethyl)phenyl)methyl)-7H-pyrrolo(3, 2-f)quinazoline-1,3-diaminePlatelet Aggregation InhibitorsPyrrolesQuinazolinesReceptor, PAR-1hypertensionmatrix metalloproteinase 1preeclampsiaprotease-activated receptor 1vasoconstriction

Identifiers

PMID26438597
PMCPMC5933188
OpenAlexW2331988875

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.