Evidence map›Paper›PMID 21806601›Full record

ArticleBritish journal of pharmacology2012

Angiotensin-(1-7) inhibits epidermal growth factor receptor transactivation via a Mas receptor-dependent pathway.

Saghir Akhtar, Mariam H M Yousif, Gursev S Dhaunsi, Bindu Chandrasekhar, Omama Al-Farsi, Ibrahim F Benter

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

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  15. Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019
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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

6 authors at 1 institution in 1 country.

Saghir AkhtarDepartment of Pharmacology and Toxicology, Faculty of Medicine, Kuwait University, Safat, Kuwait. saghir@hsc.edu.kw
Mariam H M Yousif
Gursev S Dhaunsi
Bindu Chandrasekhar
Omama Al-Farsi
Ibrahim F Benter
Kuwait University · KW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe transactivation of the epidermal growth factor (EGF) receptor appears to be an important central transduction mechanism in mediating diabetes-induced vascular dysfunction. Angiotensin-(1-7) [Ang-(1-7)] via its Mas receptor can prevent the development of hyperglycaemia-induced cardiovascular complications. Here, we investigated whether Ang-(1-7) can inhibit hyperglycaemia-induced EGF receptor transactivation and its classical signalling via ERK1/2 and p38 MAPK in vivo and in vitro. EXPERIMENTAL APPROACH: Streptozotocin-induced diabetic rats were chronically treated with Ang-(1-7) or AG1478, a selective EGF receptor inhibitor, for 4 weeks and mechanistic studies performed in the isolated mesenteric vasculature bed as well as in primary cultures of vascular smooth muscle cells (VSMCs). KEY

resultsDiabetes significantly enhanced phosphorylation of EGF receptor at tyrosine residues Y992, Y1068, Y1086, Y1148, as well as ERK1/2 and p38 MAPK in the mesenteric vasculature bed whereas these changes were significantly attenuated upon Ang-(1-7) or AG1478 treatment. In VSMCs grown in conditions of high glucose (25 mM), an Src-dependent elevation in EGF receptor phosphorylation was observed. Ang-(1-7) inhibited both Ang II- and glucose-induced transactivation of EGF receptor. The inhibition of high glucose-mediated Src-dependant transactivation of EGF receptor by Ang-(1-7) could be prevented by a selective Mas receptor antagonist, D-Pro7-Ang-(1-7). CONCLUSIONS AND IMPLICATIONS: These results show for the first time that Ang-(1-7) inhibits EGF receptor transactivation via a Mas receptor/Src-dependent pathway and might represent a novel general mechanism by which Ang-(1-7) exerts its beneficial effects in many disease states including diabetes-induced vascular dysfunction.

Indexed as

Angiotensin IAngiotensin IIAnimalsBody WeightDiabetes MellitusErbB ReceptorsGlucoseHyperglycemiaMaleMAP Kinase Signaling SystemMuscle, Smooth, VascularMyocytes, Smooth Musclep38 Mitogen-Activated Protein KinasesPeptide FragmentsPhosphorylationProto-Oncogene MasAngiotensin Iangiotensin I (1-7)Angiotensin IID-Pro7-Ang-(1-7)ErbB ReceptorsGlucosep38 Mitogen-Activated Protein KinasesPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsQuinazolinesReceptors, G-Protein-CoupledRTKI cpdsrc-Family KinasesTyrphostins

Identifiers

PMID21806601
PMCPMC3372724
OpenAlexW1594358296

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.