Evidence map›Paper›PMID 26163449›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Activation of angiotensin II type 2 receptor suppresses TNF-α-induced ICAM-1 via NF-кB: possible role of ACE2.

Liping Zhu, Oscar A Carretero, Jiang Xu, Pamela Harding, Nithya Ramadurai, Xiaosong Gu, Edward Peterson, Xiao-Ping Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  18. Effects of sevoflurane on NF-кB and TNF-α expression in renal ischemia-reperfusion diabetic rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
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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

8 authors at 1 institution in 1 country.

Liping ZhuHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and lzhu1@hfhs.org lzhu9@yahoo.com.
Oscar A CarreteroHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Jiang XuHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Pamela HardingHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Nithya RamaduraiHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Xiaosong GuHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Edward PetersonDepartment of Public Health Science, Henry Ford Hospital, Detroit, Michigan.
Xiao-Ping YangHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and.
Henry Ford Hospital · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI GARVIN, JEFFREY L. · 1985 to 2017
$39.8M
NHLBI NIH HHS HL-28982NHLBI NIH HHS P01 HL028982
6 · The paper itself

Abstract

ANG II type 2 receptor (AT2) and ANG I-converting enzyme 2 (ACE2) are important components of the renin-ANG system. Activation of AT2 and ACE2 reportedly counteracts proinflammatory effects of ANG II. However, the possible interaction between AT2 and ACE2 has never been established. We hypothesized that activation of AT2 increases ACE2 activity, thereby preventing TNF-α-stimulated ICAM-1 expression via inhibition of NF-κB signaling. Human coronary artery endothelial cells were pretreated with AT2 antagonist PD123319 (PD) or ACE2 inhibitor DX600 and then stimulated with TNF-α in the presence or absence of AT2 agonist CGP42112 (CGP). We found that AT2 agonist CGP increased both ACE2 protein expression and activity. This effect was blunted by AT2 antagonist PD. ICAM-1 expression was very low in untreated cells but greatly increased by TNF-α. Activation of AT2 with agonist CGP or with ANG II under concomitant AT1 antagonist reduced TNF-α-induced ICAM-1 expression, which was reversed by AT2 antagonist PD or ACE2 inhibitor DX600 or knockdown of ACE2 with small interfering RNA. AT2 activation also suppressed TNF-α-stimulated phosphorylation of inhibitory κB (p-IκB) and NF-κB activity. Inhibition of ACE2 reversed the inhibitory effect of AT2 on TNF-α-stimulated p-IκB and NF-κB activity. Our findings suggest that stimulation of AT2 reduces TNF-α-stimulated ICAM-1 expression, which is partly through ACE2-mediated inhibition of NF-κB signaling.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin II Type 2 Receptor BlockersCell LineCoronary VesselsEndothelial CellsHumansIntercellular Adhesion Molecule-1NF-kappa BPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 2Signal TransductionTumor Necrosis Factor-alphaACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin II Type 2 Receptor BlockersIntercellular Adhesion Molecule-1NF-kappa BPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 2Tumor Necrosis Factor-alphaANG I-converting enzyme 2ANG II type 2 receptorICAM-1TNF-α

Identifiers

PMID26163449
PMCPMC4591403
OpenAlexW2263726261

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.