Evidence map›Paper›PMID 27465439›Full record

ArticleAmerican journal of hypertension2016

Endothelin-1 Overexpression Exaggerates Diabetes-Induced Endothelial Dysfunction by Altering Oxidative Stress.

Noureddine Idris-Khodja, Sofiane Ouerd, Muhammad Oneeb Rehman Mian, Jordan Gornitsky, Tlili Barhoumi, Pierre Paradis, Ernesto L Schiffrin

Open access · bronzeAbstract read
In one paragraph

Article in American journal of hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

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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.

Noureddine Idris-KhodjaHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Sofiane OuerdHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Muhammad Oneeb Rehman MianHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Jordan GornitskyHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Tlili BarhoumiHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Pierre ParadisHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research , Montréal, Québec , Canada.
Ernesto L SchiffrinHypertension and Vascular Research Unit, Lady Davis Institute for Medical Research, Montréal, Québec, Canada.
Jewish General Hospital · CA

Funding

CIHR 102606CIHR 37917
6 · The paper itself

Abstract

backgroundIncreased endothelin (ET)-1 expression causes endothelial dysfunction and oxidative stress. Plasma ET-1 is increased in patients with diabetes mellitus. Since endothelial dysfunction often precedes vascular complications in diabetes, we hypothesized that overexpression of ET-1 in the endothelium would exaggerate diabetes-induced endothelial dysfunction.

methodsDiabetes was induced by streptozotocin treatment (55mg/kg/day, i.p.) for 5 days in 6-week-old male wild type (WT) mice and in mice overexpressing human ET-1 restricted to the endothelium (eET-1). Mice were studied 14 weeks later. Small mesenteric artery (MA) endothelial function and vascular remodeling by pressurized myography, reactive oxygen species (ROS) production by dihydroethidium staining and mRNA expression by reverse transcription/quantitative PCR were determined.

resultsEndothelium-dependent vasodilatory responses to acetylcholine of MA were reduced 24% by diabetes in WT ( P < 0.05), and further decreased by 12% in eET-1 ( P < 0.05). Diabetes decreased MA media/lumen in WT and eET-1 ( P < 0.05), whereas ET-1 overexpression increased MA media/lumen similarly in diabetic and nondiabetic WT mice ( P < 0.05). Vascular ROS production was increased 2-fold by diabetes in WT ( P < 0.05) and further augmented 1.7-fold in eET-1 ( P < 0.05). Diabetes reduced endothelial nitric oxide synthase (eNOS, Nos3 ) expression in eET-1 by 31% ( P < 0.05) but not in WT. Induction of diabetes caused a 52% ( P < 0.05) increase in superoxide dismutase 1 ( Sod1 ) and a 32% ( P < 0.05) increase in Sod2 expression in WT but not in eET-1.

conclusionsIncreased expression of ET-1 exaggerates diabetes-induced endothelial dysfunction. This may be caused by decrease in eNOS expression, increase in vascular oxidative stress, and decrease in antioxidant capacity.

Indexed as

Diabetes MellitusEndothelin-1Oxidative StressAnimalsEndothelium, VascularHumansMaleMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIReactive Oxygen SpeciesEndothelin-1Nitric OxideNitric Oxide Synthase Type IIIReactive Oxygen Species

Identifiers

PMID27465439
PMCPMC5055737
OpenAlexW2485631841

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.