Evidence map›Paper›PMID 28818856›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2017

Deletion of NF-κB/RelA in Angiotensin II-Sensitive Mesenchymal Cells Blocks Aortic Vascular Inflammation and Abdominal Aortic Aneurysm Formation.

Talha Ijaz, Hong Sun, Irina V Pinchuk, Dianna M Milewicz, Ronald G Tilton, Allan R Brasier

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 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

6 authors at 1 institution in 1 country.

Talha IjazFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.).
Hong SunFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.).
Irina V PinchukFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.).
Dianna M MilewiczFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.).
Ronald G TiltonFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.).
Allan R BrasierFrom the Department of Biochemistry and Molecular Biology (T.I.), MD-PhD Program (T.I.), Division of Gasteroenterology, Department of Internal Medicine (I.V.P.), Division of Endocrinology, Department of Internal Medicine (H.S., R.G.T., A.R.B.), Institute for Translational Sciences (R.G.T., A.R.B.), Sealy Center for Molecular Medicine (R.G.T., A.R.B.), University of Texas Medical Branch, Galveston; and Department of Internal Medicine, University of Texas Health Science Center at Houston (D.M.M.). arbrasie@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

UTMB Clinical and Translational Science AwardUL1TR001439 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI URBAN, RANDALL J · 2015 to 2024
$40.0M
Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
Center for Clinical and Translational Sciences (CCTS)UL1TR000371 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$13.4M
Pathology and Molecular Imaging CoreP01HL110869 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2012 to 2016
$10.4M
NFkB/RelA Signaling in Fibroblasts in the Development of AAA and Aortic RuptureF30HL128036 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI IJAZ, TALHA · 2015 to 2016
$68k
NCATS NIH HHS UL1 TR000371NCATS NIH HHS UL1 TR001439NHLBI NIH HHS F30 HL128036NHLBI NIH HHS P01 HL110869NIEHS NIH HHS P30 ES006676
6 · The paper itself

Abstract

objectiveInfusion of angiotensin II (Ang II) induces extracellular matrix remodeling and inflammation resulting in abdominal aortic aneurysms (AAAs) in normolipidemic mice. Although Ang II activates mesenchymal cells in the media and adventitia to become fibrogenic, the sentinel role of this mesenchymal population in modulating the inflammatory response and aneurysms is not known. We test the hypothesis that these fibrogenic mesenchymal cells play a critical role in Ang II-induced aortic wall vascular inflammation and AAA formation. APPROACH AND

resultsAng II infusion increased phospho-Ser536-RelA and interleukin (IL)-6 immunostaining in the abdominal aorta. In addition, aortic mRNA transcripts of RelA-dependent cytokines IL-6 and IL-1β were significantly elevated suggesting that Ang II functionally activates RelA signaling. To test the role of mesenchymal RelA in AAA formation, we generated RelA-CKO mice by administering tamoxifen to double transgenic mice harboring RelA-flox alleles and tamoxifen-inducible Col1a2 promoter-driven Cre recombinase (Col1a2-CreER

conclusionsFibrogenic mesenchymal RelA plays a causal role in Ang II-induced vascular inflammation and AAA in normolipidemic mice.

Indexed as

Angiotensin IIAnimalsAortaAorta, AbdominalAortic Aneurysm, AbdominalBlood PressureCollagen Type IIntegrasesMesenchymal Stem CellsMiceMice, TransgenicMonocytesTamoxifenTranscription Factor RelAAngiotensin IICol1a2 protein, mouseCollagen Type ICre recombinaseIntegrasesTamoxifenTranscription Factor RelAangiotensin IIanimalsaortic aneurysm, abdominalblood pressureinterleukin-6

Identifiers

PMID28818856
PMCPMC5620126
OpenAlexW2749038607

What OpenQuestion holds

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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.