Evidence map›Paper›PMID 31675376›Full record

ArticlePloS one2019

Ang-(1-7)/ MAS1 receptor axis inhibits allergic airway inflammation via blockade of Src-mediated EGFR transactivation in a murine model of asthma.

Ahmed Z El-Hashim, Maitham A Khajah, Rhema S Babyson, Waleed M Renno, Charles I Ezeamuzie, Ibrahim F Benter, Saghir Akhtar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. 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
2.1field-weighted citation impact, top 11% 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, 24 citations in OpenAlex.

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  8. Anti-inflammatory mechanism of rhein in treating asthma based on network pharmacology.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
    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 3 institutions in 3 countries.

Ahmed Z El-HashimDepartment of Pharmacology & Therapeutics, Faculty of Pharmacy, Kuwait University, Kuwait City, Kuwait.ORCID 0000-0002-3888-8039
Maitham A KhajahDepartment of Pharmacology & Therapeutics, Faculty of Pharmacy, Kuwait University, Kuwait City, Kuwait.
Rhema S BabysonDepartment of Pharmacology & Therapeutics, Faculty of Pharmacy, Kuwait University, Kuwait City, Kuwait.
Waleed M RennoDepartment of Anatomy, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Charles I EzeamuzieDepartment of Pharmacology and Toxicology, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Ibrahim F BenterFaculty of Medicine, Eastern Mediterranean University, Famagusta, North Cyprus.
Saghir AkhtarCollege of Medicine, Qatar University, Doha, Qatar.
Kuwait University · KWEastern Mediterranean University · CYQatar University · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The angiotensin-(1-7) [Ang-(1-7)]/MAS1 receptor signaling axis is a key endogenous anti-inflammatory signaling pathway. However, the mechanisms by which its mediates the anti-inflammatory effects are not completely understood. Using an allergic murine model of asthma, we investigated whether Ang-1(1-7)/MAS1 receptor axis a): inhibits allergic inflammation via modulation of Src-dependent transactivation of the epidermal growth factor receptor (EGFR) and downstream signaling effectors such as ERK1/2, and b): directly inhibits neutrophil and/or eosinophil chemotaxis ex vivo. Ovalbumin (OVA)-induced allergic inflammation resulted in increased phosphorylation of Src kinase, EGFR, and ERK1/2. In addition, OVA challenge increased airway cellular influx, perivascular and peribronchial inflammation, fibrosis, goblet cell hyper/metaplasia and airway hyperresponsiveness (AHR). Treatment with Ang-(1-7) inhibited phosphorylation of Src kinase, EGFR, ERK1/2, the cellular and histopathological changes and AHR. Ang-(1-7) treatment also inhibited neutrophil and eosinophil chemotaxis ex vivo. These changes were reversed following pre-treatment with A779. These data show that the anti-inflammatory actions of Ang-(1-7)/ MAS1 receptor axis are mediated, at least in part, via inhibition of Src-dependent transactivation of EGFR and downstream signaling molecules such as ERK1/2. This study therefore shows that inhibition of the Src/EGRF/ERK1/2 dependent signaling pathway is one of the mechanisms by which the Ang-(1-7)/ MAS1 receptor axis mediates it anti-inflammatory effects in diseases such as asthma.

Indexed as

Signal TransductionAngiotensin IAnimalsAsthmaBlotting, WesternBronchoalveolar Lavage FluidChemotaxis, LeukocyteDisease Models, AnimalErbB ReceptorsFluorescent Antibody TechniqueLungMaleMiceMice, Inbred BALB CPeptide FragmentsProto-Oncogene MasAngiotensin Iangiotensin I (1-7)EGFR protein, mouseErbB ReceptorsMas1 protein, mousePeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledsrc-Family Kinases

Identifiers

PMID31675376
PMCPMC6824568
OpenAlexW2988032890

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Registered trials

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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.