Evidence map›Paper›PMID 19896468›Full record

ArticleBiochemical and biophysical research communications2010

Molecular mechanisms of the antagonistic action between AT1 and AT2 receptors.

Shin-ichiro Miura, Yoshino Matsuo, Yoshihiro Kiya, Sadashiva S Karnik, Keijiro Saku

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Role of G protein coupled receptors in acute kidney injury.Cell communication and signaling : CCS · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Dimerization of ATCurrent hypertension reports · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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 2 institutions in 2 countries.

Shin-ichiro MiuraDepartment of Cardiology, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-Ku, Fukuoka 814-0180, Japan. miuras@cis.fukuoka-u.ac.jp
Yoshino Matsuo
Yoshihiro Kiya
Sadashiva S Karnik
Keijiro Saku
Fukuoka University · JPCleveland Clinic · US

Funding

Molecular Basis of Ang II Receptor FunctionsR01HL057470 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 1997 to 2013
$4.4M
Phosphoproteome and Ang II-induced VSMC Gene ExpressionR01HL083243 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2006 to 2010
$1.6M
Mechanism of Cell Death in Expressing AT2 ReceptorR01HL064845 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI KARNIK, SADASHIVA S. · 2002 to 2005
$1.4M
NHLBI NIH HHS R01 HL057470NHLBI NIH HHS R01 HL064845NHLBI NIH HHS R01 HL083243
6 · The paper itself

Abstract

Although angiotensin II (Ang II) binds to Ang II type 1 (AT(1)) and type 2 (AT(2)) receptors, AT(1) and AT(2) receptors have antagonistic actions with regard to cell signaling. The molecular mechanisms that underlie this antagonism are not well understood. We examined AT(1) and AT(2) receptor-induced signal cross-talk in the cytoplasm and the importance of the hetero-dimerization of AT(1) receptor with AT(2) receptor on the cell surface. AT(1) and AT(2) receptors showed antagonistic effects toward inositol phosphate production. AT(1) receptors mainly formed homo-dimers, rather than hetero-dimers with AT(2) receptor, on the cell surface as determined by immunoprecipitation, and subsequently induced cell signals. AT(2) receptor mainly formed homo-dimers, rather than hetero-dimers with AT(1) receptor, on the cell surface. The expression levels of homo-dimerized AT(1) receptor or AT(2) receptor on the cell surface did not change after treatment with Ang II, the AT(1) receptor antagonist telmisartan or the AT(2) receptor antagonist PD123319. Finally, AT(1) and AT(2) receptor-induced signals antagonized phospholipase C-beta(3) phosphorylation. In conclusion, Ang II-induced AT(1) receptor signals may be mainly blocked by AT(2) receptor signals through their negative cross-talk in the cytoplasm rather than by the hetero-dimerization of both receptors on the cell surface. The proper balance of the expression levels of AT(1) and AT(2) receptors might be critical for the antagonistic action between these receptors.

Indexed as

Angiotensin II Type 1 Receptor BlockersAngiotensin II Type 2 Receptor BlockersBenzimidazolesBenzoatesCell LineCell MembraneHumansImidazolesInositol PhosphatesPhospholipase C betaPhosphorylationProtein MultimerizationPyridinesReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2TelmisartanAngiotensin II Type 1 Receptor BlockersAngiotensin II Type 2 Receptor BlockersBenzimidazolesBenzoatesImidazolesInositol PhosphatesPD 123319Phospholipase C betaPyridinesReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Telmisartan

Identifiers

PMID19896468
PMCPMC3891515
OpenAlexW2125332686

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.