Evidence map›Paper›PMID 18319304›Full record

ArticleDiabetes2008

Elevated epidermal growth factor receptor phosphorylation induces resistance artery dysfunction in diabetic db/db mice.

Souad Belmadani, Desiree I Palen, Romer A Gonzalez-Villalobos, Hamid A Boulares, Khalid Matrougui

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
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  9. Article
  10. Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  11. Article
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  14. Article
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11 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

5 authors at 2 institutions in 1 country.

Souad BelmadaniDepartment of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
Desiree I Palen
Romer A Gonzalez-Villalobos
Hamid A Boulares
Khalid Matrougui
Louisiana State University Health Sciences Center New Orleans · USTulane University · US

Funding

TULANE COBRE: TRANSGENIC &GENE-TARGETED ANIMAL COREP20RR017659 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2002 to 2011
$22.1M
PARTICIPATION OF PARP-1 IN THE PATHOGENESIS OF ASTHMAR01HL072889 · NHLBI · LSU HEALTH SCIENCES CENTER · PI BOULARES, HAMID · 2004 to 2015
$3.4M
Renal Function Derangements in HypertensionR01HL026371 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAVAR, LUIS GABRIEL · 1985 to 2010
$3.4M
Mechanisms of Coronary Arteriolar Dysfunction in Type 2 DiabetesR01HL095566 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MATROUGUI, KHALID · 2010 to 2014
$1.8M
NCRR NIH HHS P20 RR017659NCRR NIH HHS P20-RR-017659NHLBI NIH HHS HL-26371NHLBI NIH HHS R01 HL026371NHLBI NIH HHS R01 HL072889NHLBI NIH HHS R01 HL095566
6 · The paper itself

Abstract

objectiveWe previously showed epidermal growth factor receptor (EGFR) transactivation to be key mechanism in the regulation of resistance artery myogenic tone. Type 2 diabetes is associated with microvascular complications. We hypothesized that elevated EGFR phosphorylation contributes to resistance artery dysfunction in type 2 diabetes. RESEARCH DESIGN AND METHODS AND

resultsDiabetic db/db and nondiabetic (control) mice were treated with EGFR inhibitor (AG1478; 10 mg x kg(-1) x day(-1)) for 2 weeks. Isolated coronary artery and mesenteric resistance artery (MRA) were mounted in an arteriograph. Pressure-induced myogenic tone was increased in MRA and coronary artery from diabetic mice and normalized by AG1478. Phenylephrine-induced contraction and nitric oxide donor-induced relaxation were similar in all groups. Endothelium-dependent relaxation in response to shear stress and acetylcholine of MRA and coronary artery from diabetic mice was altered and associated with reduced endothelial nitric oxide synthase (eNOS) expression and phosphorylation. Treated diabetic mice with AG1478 improved coronary artery and MRA endothelial function and restored eNOS expression. Immunostaining and Western blot analysis showed increased endothelial and smooth muscle cell EGFR phosphorylation of MRA and coronary artery from diabetic mouse, which was reduced by AG1478. Primary cultured endothelial cells from resistance arteries treated with high glucose for 48 h showed an increase of EGFR phosphorylation associated with eNOS expression and phosphorylation decrease in response to calcium ionophore. Pretreatment of endothelial cells with AG1478 prevented the effect of high glucose.

conclusionsThis study provides evidence of the role of elevated EGFR phosphorylation in coronary artery and MRA dysfunction in diabetic db/db mice. Therefore, EGFR should be a potential target for overcoming diabetic small artery complications.

Indexed as

AnimalsCoronary VesselsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic AngiopathiesEndothelium, VascularErbB ReceptorsMesenteric ArteriesMiceNitric Oxide Synthase Type IIIPhenylephrinePhosphorylationErbB ReceptorsNitric Oxide Synthase Type IIIPhenylephrine

Identifiers

PMID18319304
PMCPMC2758606
OpenAlexW2136433300

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.