Evidence map›Paper›PMID 24464753›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Resveratrol promotes endothelial cell wound healing under laminar shear stress through an estrogen receptor-α-dependent pathway.

Arif Yurdagul, James J Kleinedler, Marshall C McInnis, Alok R Khandelwal, Allyson L Spence, A Wayne Orr, Tammy R Dugas

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. 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
2.6field-weighted citation impact, top 10% 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, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Resveratrol-Induced Signal Transduction in Wound Healing.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Guidance Molecules in Vascular Smooth Muscle.Frontiers in physiology · 2018
    Review
  16. Article
  17. Article
  18. 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

7 authors at 1 institution in 1 country.

Arif YurdagulDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana;
James J Kleinedler
Marshall C McInnis
Alok R Khandelwal
Allyson L Spence
A Wayne Orr
Tammy R Dugas
Louisiana State University Health Sciences Center Shreveport · US

Funding

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-HL-098435
6 · The paper itself

Abstract

Restenosis is an adverse outcome of angioplasty, characterized by vascular smooth muscle cell (VSMC) hyperplasia. However, therapies targeting VSMC proliferation delay re-endothelialization, increasing the risk of thrombosis. Resveratrol (RESV) inhibits restenosis and promotes re-endothelialization after arterial injury, but in vitro studies assessing RESV-mediated effects on endothelial cell growth contradict these findings. We thus hypothesized that fluid shear stress, mimicking physiological blood flow, would recapitulate RESV-dependent endothelial cell wound healing. Since RESV is an estrogen receptor (ER) agonist, we tested whether RESV promotes re-endothelialization through an ER-α-dependent mechanism. Mice fed a high-fat diet or a diet supplemented with RESV were subjected to carotid artery injury. At 7 days after injury, RESV significantly accelerated re-endothelialization compared with vehicle. In vitro wound healing assays demonstrated that RESV exhibits cell-type selectivity, inhibiting VSMC, but not endothelial cell growth. Under laminar shear stress (LSS), RESV dramatically enhanced endothelial cell wound healing and increased both the activation of extracellular signal-regulated kinase (ERK) and endothelial cell proliferation. Under LSS, small interfering RNA against ER-α, but not endothelial nitric oxide synthase, abolished RESV-induced ERK activation, endothelial cell proliferation, and wound healing. Thus these studies suggest that the EC phenotype induced by LSS better models the prohealing effects of RESV and that RESV and LSS interact to promote an ER-α-dependent mitogenic effect in endothelial cells.

Indexed as

AnimalsCardiovascular AgentsCarotid ArteriesCell ProliferationEndothelium, VascularEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesFemaleIn Vitro TechniquesMiceMice, Inbred StrainsModels, AnimalNitric Oxide Synthase Type IIIPaclitaxelRegional Blood FlowResveratrolCardiovascular AgentsEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesNitric Oxide Synthase Type IIIPaclitaxelResveratrolStilbenesendothelialestrogen receptorresveratrolsheer stresswound healing

Identifiers

PMID24464753
PMCPMC3949046
OpenAlexW2138549784

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.