Evidence map›Paper›PMID 28082260›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2017

Mechanisms of Mas1 Receptor-Mediated Signaling in the Vascular Endothelium.

Brian R Hoffmann, Timothy J Stodola, Jordan R Wagner, Daniela N Didier, Eric C Exner, Julian H Lombard, Andrew S Greene

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023
    Review
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  15. Review
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  17. Review
  18. ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020
    Review
  19. Article
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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.

Brian R HoffmannFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Timothy J StodolaFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Jordan R WagnerFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Daniela N DidierFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Eric C ExnerFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Julian H LombardFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee.
Andrew S GreeneFrom the Department of Medicine, Division of Cardiology (B.R.H.), the Department of Biomedical Engineering (B.R.H., A.S.G.), and the Department of Physiology (T.J.S., J.R.W., J.H.L., D.N.D., E.C.E., A.S.G.), Cardiovascular Center (B.R.H.), Medical College of Wisconsin, Milwaukee. agreene@mcw.edu.
Medical College of Wisconsin · US

Funding

Research ServicesP01HL082798 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W · 2006 to 2015
$22.0M
INTEGRATED PHYSIOLOGY TRAINING--MOLECULE TO ORGANISMT32HL007852 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Matthew Robert Hodges · 1996 to 2026
$6.5M
Medical Scientist Training ProgramT32GM080202 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI BARBIERI, JOSEPH T, SALZMAN, NITA H · 2010 to 2024
$5.7M
HIGH SALT DIET, ANGIOTENSIN II, AND MICROVESSEL DILATIONR01HL065289 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 2000 to 2012
$3.8M
Role of Nrf2 in Vascular Antioxidant DefenseR01HL128242 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 2016 to 2019
$1.8M
Inflammation and Infection in Acquired & Congenital Cardiovascular DiseaseT32HL094273 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GREENE, ANDREW S. · 2009 to 2013
$850k
Oxidant Stress in the Nrf2 Knockout RatR21OD018309 · OD · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 2014 to 2015
$416k
Evaluation of Endothelial Hyperglycemia-Driven Alterations During Type 2 DiabetesK01DK105043 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI HOFFMANN, BRIAN ROBERT · 2015 to 2018
$407k
Development of Mas Receptor Knockout Rat ResourceR21OD024781 · OD · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 2017 to 2018
$402k
Medhanism of EPC Dysfunction in the SS Rat: Quantity over QualityF30HL131153 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI EXNER, ERIC C · 2016 to 2019
$181k
NHLBI NIH HHS F30 HL131153NHLBI NIH HHS N01 HV028182NHLBI NIH HHS P01 HL082798NHLBI NIH HHS R01 HL065289NHLBI NIH HHS R01 HL128242NHLBI NIH HHS T32 HL007852NHLBI NIH HHS T32 HL094273NIDDK NIH HHS K01 DK105043NIDDK NIH HHS L30 DK110850NIGMS NIH HHS T32 GM080202NIH HHS R21 OD018309NIH HHS R21 OD024781
6 · The paper itself

Abstract

objectiveAngiotensin II (AngII) has been shown to regulate angiogenesis and at high pathophysiological doses to cause vasoconstriction through the AngII receptor type 1. Angiotensin 1 to 7 (Ang-(1-7)) acting through the Mas1 receptor can act antagonistically to high pathophysiological levels of AngII by inducing vasodilation, whereas the effects of Ang-(1-7) signaling on angiogenesis are less defined. To complicate the matter, there is growing evidence that a subpressor dose of AngII produces phenotypes similar to Ang-(1-7). APPROACH AND

resultsThis study shows that low-dose Ang-(1-7), acting through the Mas1 receptor, promotes angiogenesis and vasodilation similar to a low, subpressor dose of AngII acting through AngII receptor type 1. In addition, we show through in vitro tube formation that Ang-(1-7) augments the angiogenic response in rat microvascular endothelial cells. Using proteomic and genomic analyses, downstream components of Mas1 receptor signaling were identified, including Rho family of GTPases, phosphatidylinositol 3-kinase, protein kinase D1, mitogen-activated protein kinase, and extracellular signal-related kinase signaling. Further experimental antagonism of extracellular signal-related kinases 1/2 and p38 mitogen-activated protein kinase signaling inhibited endothelial tube formation and vasodilation when stimulated with equimolar, low doses of either AngII or Ang-(1-7).

conclusionsThese results significantly expand the known Ang-(1-7)/Mas1 receptor signaling pathway and demonstrate an important distinction between the pathological effects of elevated and suppressed AngII compared with the beneficial effects of AngII normalization and Ang-(1-7) administration. The observed convergence of Ang-(1-7)/Mas1 and AngII/AngII receptor type 1 signaling at low ligand concentrations suggests a nuanced regulation in vasculature. These data also reinforce the importance of mitogen-activated protein kinase/extracellular signal-related kinase signaling in maintaining vascular function.

Indexed as

Neovascularization, PhysiologicSignal TransductionVasodilationAngiotensin IAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsDose-Response Relationship, DrugElectric StimulationEndothelial CellsEndothelium, VascularExtracellular Signal-Regulated MAP KinasesGene Expression RegulationMaleMiddle Cerebral Arteryp38 Mitogen-Activated Protein KinasesAngiotensin Iangiotensin I (1-7)Angiotensin IIAngiotensin II Type 1 Receptor BlockersExtracellular Signal-Regulated MAP KinasesMas1 protein, ratp38 Mitogen-Activated Protein KinasesPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 1Receptors, G-Protein-Coupledangiotensin IIendothelium, vascularphenotyperenin-angiotensin systemvasodilation

Identifiers

PMID28082260
PMCPMC5323371
OpenAlexW2892644088

What OpenQuestion holds

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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.