Evidence map›Paper›PMID 2154969›Full record

ArticleThe Biochemical journal1990

Cholera toxin modulation of angiotensin II-stimulated inositol phosphate production in cultured vascular smooth muscle cells.

L Socorro, R W Alexander, K K Griendling

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

4 citing papers in PubMed, 35 citations in OpenAlex.

  1. 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

3 authors at 1 institution in 1 country.

L SocorroDepartment of Medicine, Brigham and Women's Hospital, Boston, MA.
R W Alexander
K K Griendling
Harvard University · US

Funding

NOX4 and vascular smooth muscle differentiationR37HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 2006 to 2015
$3.8M
VASCULAR SMOOTH MUSCLE PHOSPHOLIPASE DR01HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 1993 to 2005
$2.1M
VASCULAR SMOOTH MUSCLE CELLS: PATHOPHYSIOLOGYR01HL035013 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A · 1985 to 1991
–
DIACYLGLYCEROL SIGNALING IN VASCULAR SMOOTH MUSCLER29HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 1987 to 1991
–
NHLBI NIH HHS HL35013NHLBI NIH HHS HL38206
6 · The paper itself

Abstract

Activation of phospholipase C by angiotensin II in vascular smooth muscle has been postulated to be mediated by an unidentified GTP-binding protein (G-protein). Using a permeabilized preparation of myo-[3H]inositol-labelled cultured vascular smooth muscle cells, we examined the ability of a non-hydrolysable analogue of GTP, guanosine 5'-[gamma-thio]triphosphate (GTP[S]), to stimulate inositol phosphate formation. GTP[S] (5 min exposure) stimulated inositol polyphosphate release by up to 3.8-fold in a dose-dependent manner, with an EC50 (concn. producing half-maximal stimulation) of approx. 50 microM. Inositol bisphosphate (IP2) and inositol trisphosphate (IP3) accumulations were also stimulated by NaF (5-20 mM). Furthermore, angiotensin II-induced inositol phosphate formation could be potentiated by a submaximal concentration of GTP[S] (10 microM), and this treatment appeared to interfere with the normal termination mechanism of the initial hormonal signal. The G-protein mediating angiotensin II-stimulated phospholipase C activation was insensitive to pertussis toxin at an exposure time and concentration which were sufficient to completely ADP-ribosylate all available substrate (100 ng/ml, 16 h). In contrast, a similar incubation with cholera toxin markedly inhibited angiotensin II-stimulated IP2 and IP3 release by 67 +/- 6% and 62 +/- 6% respectively. Cholera toxin appeared to inhibit angiotensin II stimulation of phospholipase C by a dual mechanism: it caused a 45% decrease in angiotensin II receptor number, and also inhibited G-protein transduction as assessed by GTP[S]-stimulated IP2 formation. This latter inhibition may be secondary to an increase in cyclic AMP, since it could be simulated by addition of dibutyryl cyclic AMP. Thus angiotensin II-stimulated inositol phosphate formation is cholera-toxin-sensitive, and is mediated by a pertussis-toxin-insensitive G-protein, which may be involved directly in termination of early signal generation.

Indexed as

Adenosine Diphosphate RiboseAngiotensin IIAnimalsBucladesineCalciumCells, CulturedCholera ToxinDepression, ChemicalElectrophoresis, Polyacrylamide GelEndothelium, VascularGuanosine 5'-O-(3-Thiotriphosphate)Guanosine TriphosphateInositol 1,4,5-TrisphosphateRatsReceptors, AngiotensinSodium FluorideAdenosine Diphosphate RiboseAngiotensin IIBucladesineCalciumCholera ToxinGuanosine 5'-O-(3-Thiotriphosphate)Guanosine TriphosphateInositol 1,4,5-TrisphosphateReceptors, AngiotensinSodium FluorideThionucleotides

Identifiers

PMID2154969
PMCPMC1133703
OpenAlexW2415244100

What OpenQuestion holds

Textmetadata
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.