Evidence map›Paper›PMID 30383775›Full record

ArticlePloS one2018

Mechanism of anti-remodelling action of treprostinil in human pulmonary arterial smooth muscle cells.

Christopher Lambers, Christoph Kornauth, Felicitas Oberndorfer, Panja M Boehm, Michael Tamm, Walter Klepetko, Michael Roth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
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  9. Effect of Treprostinil on the Early Postoperative Prognosis of Patients with Severe Left Heart Valvular Disease Combined with Severe Pulmonary Hypertension.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2021
    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 2 countries.

Christopher LambersThoracic Surgery, University Hospital Vienna, Vienna, Austria.
Christoph KornauthClinical Institute of Pathology, Medical University of Vienna, Vienna, Austria.
Felicitas OberndorferClinical Institute of Pathology, Medical University of Vienna, Vienna, Austria.
Panja M BoehmThoracic Surgery, University Hospital Vienna, Vienna, Austria.ORCID 0000-0002-7762-5477
Michael TammPulmonary Cell Research and Pneumology Clinics, University and University Hospital Basel, Basel, Switzerland.
Walter KlepetkoThoracic Surgery, University Hospital Vienna, Vienna, Austria.
Michael RothPulmonary Cell Research and Pneumology Clinics, University and University Hospital Basel, Basel, Switzerland.ORCID 0000-0002-8139-2821
Vienna General Hospital · ATMedical University of Vienna · ATUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treprostinil is applied for pulmonary arterial hypertension (PAH) therapy. However, the mechanism by which the drug achieves its beneficial effects in PAH vessels is not fully understood. This study investigated the effects of treprostinil on PDGF-BB induced remodelling parameters in isolated human pulmonary arterial smooth muscle cells (PASMC) of four PAH patients. The production of TGF-β1, CTGF, collagen type-I and -IV, and of fibronectin were determined by ELISA and PCR. The role of cAMP was determined by ELISA and di-deoxyadenosine treatment. Proliferation was determined by direct cell count. Treprostinil increased cAMP levels dose and time dependently, which was not affected by PDGF-BB. Treprostinil significantly reduced PDGF-BB induced secretion of TGF-β1 and CTGF, both was counteracted when cAMP generation was blocked. Similarly, the PDGF-BB induced proliferation of PASMC was dose dependently reduced by treprostinil through signalling via cAMP-C/EBP-α p42 -p21(WAf1/Cip1). In regards to extracellular matrix remodelling, treprostinil significantly reduced PDGF-BB-TGF-β1-CTGF induced synthesis and deposition of collagen type I and fibronectin, in a cAMP sensitive manner. In contrast, the deposition of collagen IV was not affected. The data suggest that this action of treprostinil in vessel wall remodelling may benefit patients with PAH and may reduce arterial wall remodelling.

Indexed as

AdultBecaplerminCCAAT-Enhancer-Binding ProteinsCell ProliferationCollagen Type ICollagen Type IVConnective Tissue Growth FactorCyclic AMPEpoprostenolExtracellular MatrixFamilial Primary Pulmonary HypertensionFemaleFibronectinsGene Expression RegulationHumansMaleBecaplerminCCAAT-Enhancer-Binding ProteinsCCN2 protein, humanCEBPA protein, humanCollagen Type ICollagen Type IVConnective Tissue Growth FactorCyclic AMPEpoprostenolFibronectinsFN1 protein, humanMitogen-Activated Protein Kinase 1Transforming Growth Factor beta1treprostinil

Identifiers

PMID30383775
PMCPMC6211661
OpenAlexW2899003343

What OpenQuestion holds

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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.