Evidence map›Paper›PMID 35643499›Full record

ArticleRespiratory research2022

Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation.

Abdullah A Alqarni, Oliver J Brand, Alice Pasini, Mushabbab Alahmari, Abdulrhman Alghamdi, Linhua Pang

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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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 2 institutions in 2 countries.

Abdullah A AlqarniRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK.
Oliver J BrandRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK.
Alice PasiniRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK.
Mushabbab AlahmariRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK.
Abdulrhman AlghamdiRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK.
Linhua PangRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, City Hospital Campus, Nottingham, NG5 1PB, UK. linhua.pang@nottingham.ac.uk.
University of Nottingham · GBKing Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary hypertension is a common and serious complication of chronic obstructive pulmonary disease (COPD). Studies suggest that cigarette smoke can initiate pulmonary vascular remodelling by stimulating cell proliferation; however, the underlying cause, particularly the role of vasoactive prostanoids, is unclear. We hypothesize that cigarette smoke extract (CSE) can induce imbalanced vasoactive prostanoid release by differentially modulating the expression of respective synthase genes in human pulmonary artery smooth muscle cells (PASMCs) and endothelial cells (PAECs), thereby contributing to cell proliferation.

methodsAqueous CSE was prepared from 3R4F research-grade cigarettes. Human PASMCs and PAECs were treated with or without CSE. Quantitative real-time RT-PCR and Western blotting were used to analyse the mRNA and protein expression of vasoactive prostanoid syhthases. Prostanoid concentration in the medium was measured using ELISA kits. Cell proliferation was assessed using the cell proliferation reagent WST-1.

resultsWe demonstrated that CSE induced the expression of cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostanoid synthesis, in both cell types. In PASMCs, CSE reduced the downstream prostaglandin (PG) I synthase (PGIS) mRNA and protein expression and PGI

conclusionsThese findings provide the first evidence that cigarette smoke can induce imbalanced prostanoid mediator release characterized by the reduced PGI

Indexed as

Cigarette SmokingHypertension, PulmonaryPulmonary Disease, Chronic ObstructiveCell ProliferationEndothelial CellsHumansNicotianaProstaglandinsProstaglandins EPulmonary ArteryRNA, MessengerVascular RemodelingProstaglandinsProstaglandins ERNA, MessengerCigarette smokeCOPDProstanoidsPulmonary artery cell proliferationPulmonary hypertension

Identifiers

PMID35643499
PMCPMC9145181
OpenAlexW4281937944

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.