Evidence map›Paper›PMID 27550920›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Heteromerization Between the Bradykinin B2 Receptor and the Angiotensin-(1-7) Mas Receptor: Functional Consequences.

Bruno D Cerrato, Oscar A Carretero, Brana Janic, Hernán E Grecco, Mariela M Gironacci

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Angiotensin ATJournal of neuroinflammation · 2020
    Article
  7. The Vasoactive Mas Receptor in Essential Hypertension.Journal of clinical medicine · 2020
    Review
  8. Review
  9. Article
  10. Article
  11. The Meaning of Mas.Hypertension (Dallas, Tex. : 1979) · 2018
    Review
  12. Article
  13. Review
  14. Review
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

5 authors at 1 institution in 1 country.

Bruno D CerratoFrom the Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina (B.D.C., M.M.G.); Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI (O.A.C., B.J.); and Departamento de Física, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBA-CONICET, Argentina (H.E.G).
Oscar A CarreteroFrom the Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina (B.D.C., M.M.G.); Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI (O.A.C., B.J.); and Departamento de Física, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBA-CONICET, Argentina (H.E.G).
Brana JanicFrom the Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina (B.D.C., M.M.G.); Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI (O.A.C., B.J.); and Departamento de Física, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBA-CONICET, Argentina (H.E.G).
Hernán E GreccoFrom the Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina (B.D.C., M.M.G.); Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI (O.A.C., B.J.); and Departamento de Física, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBA-CONICET, Argentina (H.E.G).
Mariela M GironacciFrom the Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina (B.D.C., M.M.G.); Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI (O.A.C., B.J.); and Departamento de Física, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBA-CONICET, Argentina (H.E.G). mariela@qb.ffyb.uba.ar.
Instituto de Química y Fisicoquímica Biológicas · AR

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 P01 HL028982
6 · The paper itself

Abstract

Bradykinin B2 receptor (B2R) and angiotensin-(1-7) Mas receptor (MasR)-mediated effects are physiologically interconnected. The molecular basis for such cross talk is unknown. It is hypothesized that the cross talk occurs at the receptor level. We investigated B2R-MasR heteromerization and the functional consequences of such interaction. B2R fused to the cyan fluorescent protein and MasR fused to the yellow fluorescent protein were transiently coexpressed in human embryonic kidney293T cells. Fluorescence resonance energy transfer analysis showed that B2R and MasR formed a constitutive heteromer, which was not modified by their agonists. B2R or MasR antagonists decreased fluorescence resonance energy transfer efficiency, suggesting that the antagonist promoted heteromer dissociation. B2R-MasR heteromerization induced an 8-fold increase in the MasR ligand-binding affinity. On agonist stimulation, the heteromer was internalized into early endosomes with a slower sequestration rate from the plasma membrane, compared with single receptors. B2R-MasR heteromerization induced a greater increase in arachidonic acid release and extracellular signal-regulated kinase phosphorylation after angiotensin-(1-7) stimulation, and this effect was blocked by the B2R antagonist. Concerning serine/threonine kinase Akt activity, a significant bradykinin-promoted activation was detected in B2R-MasR but not in B2R-expressing cells. Angiotensin-(1-7) and bradykinin elicited antiproliferative effects only in cells expressing B2R-MasR heteromers, but not in cells expressing each receptor alone. Proximity ligation assay confirmed B2R-MasR interaction in human glomerular endothelial cells supporting the interaction between both receptors in vivo. Our findings provide an explanation for the cross talk between bradykinin B2R and angiotensin-(1-7) MasR-mediated effects. B2R-MasR heteromerization induces functional changes in the receptor that may lead to long-lasting protective properties.

Indexed as

Analysis of VarianceAngiotensin IAnimalsBradykinin B2 Receptor AntagonistsCell MembraneCells, CulturedExtracellular Signal-Regulated MAP KinasesHEK293 CellsHumansPeptide FragmentsProto-Oncogene MasRatsReceptor, Bradykinin B2Receptor Cross-TalkRenin-Angiotensin SystemSensitivity and SpecificityAngiotensin Iangiotensin I (1-7)Bradykinin B2 Receptor AntagonistsExtracellular Signal-Regulated MAP KinasesMAS1 protein, humanPeptide FragmentsProto-Oncogene MasReceptor, Bradykinin B2B2 receptorheteromerizationMas receptor

Identifiers

PMID27550920
PMCPMC5016258
OpenAlexW2588810449

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.