Evidence map›Paper›PMID 41159679›Full record

ArticleComprehensive Physiology2025

Disrupting BMP/TGF-β Signaling: Modulation of AQP1 and TGFB1 in Human Pulmonary Microvascular Endothelial Cells.

Chrysi Keskinidou, Nikolaos S Lotsios, Kostas A Papavassiliou, Athanasios G Papavassiliou, Ioanna Dimopoulou, Anastasia Kotanidou, David Langleben, Stylianos E Orfanos, Alice G Vassiliou

Abstract read
In one paragraph

Article in Comprehensive Physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Chrysi KeskinidouFirst Department of Critical Care Medicine, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, Athens, Greece.ORCID 0000-0002-4047-3588
Nikolaos S LotsiosFirst Department of Critical Care Medicine, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, Athens, Greece.ORCID 0000-0002-7194-3976
Kostas A PapavassiliouFirst University Department of Respiratory Medicine, 'Sotiria' Chest Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.ORCID 0000-0001-9620-745X
Athanasios G PapavassiliouDepartment of Biological Chemistry, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.ORCID 0000-0001-5803-4527
Ioanna DimopoulouFirst Department of Critical Care Medicine, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, Athens, Greece.ORCID 0000-0002-2219-7292
Anastasia KotanidouFirst Department of Critical Care Medicine, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, Athens, Greece.ORCID 0000-0003-4703-0082
David LanglebenCenter for Pulmonary Vascular Disease, Azrieli Heart Center and Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, Quebec, Canada.ORCID 0000-0002-6495-0094
Stylianos E OrfanosSchool of Medicine, National and Kapodistrian University of Athens, Athens, Greece.ORCID 0000-0002-7760-4895
Alice G VassiliouFirst Department of Critical Care Medicine, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, Athens, Greece.ORCID 0000-0003-4984-0476

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a chronic disorder with high fatality rates, and its progression is highly associated with the genetic background. Alongside pathogenic variants in genes central to the BMP/TGF-β signaling pathway, recent evidence has linked aquaporin 1 (AQP1) gene variants to PAH. While BMP9 shows promise as a PAH therapy, emerging conflicting evidence challenges this prospect. Herein, we modulated the gene expression of AQP1 and TGFB1 and examined their effect, before and after BMP9 administration, on BMP9, BMP10, BMPR2, AQP1, TGFBR1, and TGFB1 in human pulmonary microvascular endothelial cells (HPMECs) in vitro. Our results demonstrated that silencing of the AQP1 gene resulted in decreased BMPR2 mRNA and protein, downregulated TGFB1 and TGFBR1 mRNA, while tending to reduce TGFBR1 protein levels. BMP9 exogenous administration affected only TGFB1 mRNA, restoring control levels. Silencing of the TGFB1 gene downregulated BMPR2 mRNA and protein levels and affected the expression of its ligands; BMP9 mRNA and protein increased, while BMP10 mRNA levels decreased. Exogenous BMP9 treatment of TGFB1-silenced cells decreased AQP1 mRNA and protein levels. Our results indicate that modulation of AQP1 and TGFB1 genes could possibly disrupt the complex signaling pathway, and that the effects of BMP9 may be cell- and context-dependent. Together, these findings could provide a novel perspective on the interactions of the BMP/TGF-β signaling pathway.

Indexed as

Aquaporin 1Endothelial CellsLungTransforming Growth Factor beta1Bone Morphogenetic Protein Receptors, Type IICells, CulturedHumansMicrovesselsReceptor, Transforming Growth Factor-beta Type ISignal TransductionAQP1 protein, humanAquaporin 1Bone Morphogenetic Protein Receptors, Type IIReceptor, Transforming Growth Factor-beta Type ITGFB1 protein, humanTransforming Growth Factor beta1AQP1BMP9BMPR2PAHTGF‐β

Identifiers

PMID41159679
PMCPMC12570780

What Socratic holds

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LicenceCC BY
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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 Socratic graph.