Evidence map›Paper›PMID 32576665›Full record

ArticleJournal of cell science2020

Endothelial protective factors BMP9 and BMP10 inhibit CCL2 release by human vascular endothelial cells.

Paul D Upton, John E S Park, Patricia M De Souza, Rachel J Davies, Mark J D Griffiths, Stephen J Wort, Nicholas W Morrell

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Bone morphogenetic protein 10: clinical correlates and risk of incident atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  2. Article
  3. Bone morphogenetic protein-9 controls pulmonary vascular growth and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. An emerging class of new therapeutics targeting TGF, Activin, and BMP ligands in pulmonary arterial hypertension.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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 2 institutions in 2 countries.

Paul D UptonUniversity of Cambridge School of Clinical Medicine, Addenbrooke's/CUHNHSFT and Papworth Hospitals, Cambridge CB2 0QQ, UK pdu21@medschl.cam.ac.uk.ORCID 0000-0003-2716-4921
John E S ParkUnit of Critical Care, NHLI, Imperial College, London SW3 6LY, UK.
Patricia M De SouzaUnit of Critical Care, NHLI, Imperial College, London SW3 6LY, UK.ORCID 0000-0002-7072-0340
Rachel J DaviesUnit of Critical Care, NHLI, Imperial College, London SW3 6LY, UK.
Mark J D GriffithsUnit of Critical Care, NHLI, Imperial College, London SW3 6LY, UK.
Stephen J WortUnit of Critical Care, NHLI, Imperial College, London SW3 6LY, UK.
Nicholas W MorrellUniversity of Cambridge School of Clinical Medicine, Addenbrooke's/CUHNHSFT and Papworth Hospitals, Cambridge CB2 0QQ, UK.
Imperial College London · GBUniversity of Cambridge · GB

Funding

British Heart Foundation RG/08/002/24718British Heart Foundation RG/13/4/30107Department of HealthMedical Research Council G0701361Wellcome TrustWellcome Trust GR077167MA
6 · The paper itself

Abstract

Bone morphogenetic protein 9 (BMP9) and BMP10 are circulating ligands that mediate endothelial cell (EC) protection via complexes of the type I receptor ALK1 and the type II receptors activin type-IIA receptor (ACTR-IIA) and bone morphogenetic type II receptor (BMPR-II). We previously demonstrated that BMP9 induces the expression of interleukin-6, interleukin-8 and E-selectin in ECs and might influence their interactions with monocytes and neutrophils. We asked whether BMP9 and BMP10 regulate the expression of chemokine (C-C motif) ligand 2 (CCL2), a key chemokine involved in monocyte-macrophage chemoattraction. Here, we show that BMP9 and BMP10 repress basal CCL2 expression and release from human pulmonary artery ECs and aortic ECs. The repression was dependent on ALK1 and co-dependent on ACTR-IIA and BMPR-II. Assessment of canonical Smad signalling indicated a reliance of this response on Smad4. Of note, Smad1/5 signalling contributed only at BMP9 concentrations similar to those in the circulation. In the context of inflammation, BMP9 did not alter the induction of CCL2 by TNF-α. As CCL2 promotes monocyte/macrophage chemotaxis and endothelial permeability, these data support the concept that BMP9 preserves basal endothelial integrity.

Indexed as

Endothelial CellsGrowth Differentiation Factor 2Activin Receptors, Type IIBone Morphogenetic ProteinsChemokine CCL2HumansProtective FactorsActivin Receptors, Type IIBMP10 protein, humanBone Morphogenetic ProteinsCCL2 protein, humanChemokine CCL2GDF2 protein, humanGrowth Differentiation Factor 2BMP10BMP9CCL2Endothelial cellsTNF

Identifiers

PMID32576665
PMCPMC7390625
OpenAlexW3038116671

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.