Evidence map›Paper›PMID 18255343›Full record

ArticleVascular pharmacology

Inhibition of vascular inflammation by dehydroepiandrosterone sulfate in human aortic endothelial cells: roles of PPARalpha and NF-kappaB.

Robin Altman, Deborah D Motton, Rama S Kota, John C Rutledge

Abstract read
In one paragraph

Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.7field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  8. Menopause, androgens, and cardiovascular ageing: a narrative review.Therapeutic advances in endocrinology and metabolism · 2022
    Review
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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

4 authors at 3 institutions in 1 country.

Robin AltmanDivision of Endocrinology, Department of Internal Medicine, School of Medicine, University of California, Davis, CA 95616, United States. raltman@ucdavis.edu
Deborah D Motton
Rama S Kota
John C Rutledge
University of California, Davis · USUniversity of California, Merced · USUniversity of California System · US

Funding

Interactions of Lipoproteins with the Vascular WallR01HL055667 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI RUTLEDGE, JOHN CALVERT · 1996 to 2010
$2.8M
USE OF POSITRON TOMOGRAPHY (PET) TO STUDY FRONTOTEMPORAL DEMENTIASM01RR019975 · NCRR · UNIVERSITY OF CALIFORNIA DAVIS · PI POMEROY, CLAIRE · 2004 to 2006
$2.5M
Brain Microvascular Determinants of Alzheimers DiseaseR01AG039094 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI RUTLEDGE, JOHN CALVERT · 2010 to 2014
$2.1M
Effects of a high glycemic load diet on vascular systemR01HL071488 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI RUTLEDGE, JOHN CALVERT · 2002 to 2003
$641k
NCRR NIH HHS M01 RR019975NHLBI NIH HHS HL55667NHLBI NIH HHS R01 HL055667NHLBI NIH HHS R01 HL071488NIA NIH HHS R01 AG039094
6 · The paper itself

Abstract

Dehydroepiandrosterone sulfate (DHEAS) is a hormone produced by the adrenal gland and is a precursor for both androgens and estrogens. Atherosclerosis is a well characterized inflammatory disease, but little is known about the role of DHEAS in vascular inflammation. We hypothesize that DHEAS can reduce inflammation in vascular endothelial cells and the mechanism involves the peroxisome proliferator-activated receptor alpha (PPARalpha), thereby inhibiting transcription factors involved in endothelial cell inflammation. To test our hypothesis, aortic endothelial cells were pretreated for 48 h with DHEAS, then with TNF-alpha. TNF-alpha-induced upregulation of the expression of inflammatory genes interleukin (IL)-8 and intracellular adhesion molecule (ICAM)-1 was attenuated by incubation with DHEAS. DHEAS inhibited the TNF-alpha-induced surface expression of vascular cell adhesion molecule (VCAM)-1. This effect was abolished by the addition of MK866, a PPARalpha inhibitor, indicating that PPARalpha is involved in the mechanism of this inhibition. The addition of the aromatase inhibitor letrozole had no effect on the inhibition of TNF-alpha-induced VCAM-1 expression by DHEAS. Treatment of endothelial cells with DHEAS dramatically inhibited the TNF-alpha-induced activation of NF-kappaB, an inflammatory transcription factor, and increased protein levels of the NF-kappaB inhibitor, IkappaB-alpha. These results signify the ability of DHEAS to directly inhibit the inflammatory process and show a potential direct effect of DHEAS on vascular inflammation that has implications for the development of atherosclerotic cardiovascular disease.

Indexed as

AortaAromatase InhibitorsCell SurvivalDehydroepiandrosterone SulfateEndothelial CellsEstradiolEstrogen AntagonistsFulvestrantHumansI-kappa B ProteinsInflammationIntercellular Adhesion Molecule-1Interleukin-8LetrozoleNF-kappa BNF-KappaB Inhibitor alphaAromatase InhibitorsDehydroepiandrosterone SulfateEstradiolEstrogen AntagonistsFulvestrantI-kappa B ProteinsIntercellular Adhesion Molecule-1Interleukin-8LetrozoleNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNitrilesPPAR alphaTriazolesTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID18255343
PMCPMC3656484
OpenAlexW2081225653

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.