Evidence map›Paper›PMID 26160957›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Fibroblast Angiotensin II Type 1a Receptors Contribute to Angiotensin II-Induced Medial Hyperplasia in the Ascending Aorta.

Aruna Poduri, Debra L Rateri, Deborah A Howatt, Anju Balakrishnan, Jessica J Moorleghen, Lisa A Cassis, Alan Daugherty

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-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

38 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Phospholipase Cε insufficiency causes ascending aortic aneurysm and dissection.American journal of physiology. Heart and circulatory physiology · 2022
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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.

Aruna PoduriFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Debra L RateriFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Deborah A HowattFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Anju BalakrishnanFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Jessica J MoorleghenFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Lisa A CassisFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington.
Alan DaughertyFrom the Saha Cardiovascular Research Center (A.P., D.L.R., D.A.H., A.B., J.J.M., A.D.) and Department of Molecular and Biomedical Pharmacology (L.A.C.), University of Kentucky, Lexington. Alan.Daugherty@uky.edu.
University of Kentucky · US

Funding

Mechanisms of thoracic aortic aneurysmsR01HL107319 · NHLBI · UNIVERSITY OF KENTUCKY · PI DAUGHERTY, ALAN · 2012 to 2015
$2.1M
NHLBI NIH HHS HL107319NHLBI NIH HHS R01 HL107319
6 · The paper itself

Abstract

objectiveAngiotensin II (Ang II) infusion causes aortic medial thickening via stimulation of angiotensin II type 1a (AT1a) receptors. The purpose of this study was to determine the cellular loci of AT1a receptors that mediate this Ang II-induced aortic pathology. APPROACH AND

resultsSaline or Ang II was infused into AT1a receptor floxed mice expressing Cre under control of cell-specific promoters. Initially, AT1a receptors were depleted in aortic smooth muscle cell and endothelium by expressing Cre under control of SM22 and Tie2 promoters, respectively. Deletion of AT1a receptors in either cell type had no effect on Ang II-induced medial thickening. To determine whether this effect was related to neural stimulation, AT1a receptors were depleted using an enolase 2-driven Cre. Depletion of AT1a receptors in neural cells attenuated Ang II-induced medial thickening of the ascending, but not descending aorta. Lineage tracking studies, using ROSA26-LacZ, demonstrated that enolase 2 was also expressed in adventitial cells adjacent to the region of attenuated thickening. To determine whether adventitial fibroblasts contributed to this attenuation, AT1a receptors in fibroblasts were depleted using S100A4 driven Cre. Similar to enolase 2-Cre, Ang II-induced medial thickening was attenuated in the ascending, but not the descending aorta. Lineage tracking demonstrated an increase of S100A4-LacZ positive cells in the media of the ascending region during Ang II infusion.

conclusionsAT1a receptor depletion in fibroblasts attenuates Ang II-induced medial hyperplasia in the ascending aorta.

Indexed as

Gene Expression RegulationAngiotensin IIAnimalsAorta, ThoracicAtherosclerosisDisease Models, AnimalDNAFibroblastsGenotypeHyperplasiaInfusions, IntravenousMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Angiotensin, Type 1Angiotensin IIDNAReceptor, Angiotensin, Type 1RNA, Messengerangiotensin IIangiotensin II type 1 receptorendotheliumfibroblastsmedial thickeningsmooth muscle

Identifiers

PMID26160957
PMCPMC4552596
OpenAlexW2153027368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.