Evidence map›Paper›PMID 31075112›Full record

ArticlePloS one2019

GDF15 secreted by senescent endothelial cells improves vascular progenitor cell functions.

Guillaume Ha, Fanny De Torres, Nassim Arouche, Nassima Benzoubir, Ségolène Ferratge, Elie Hatem, Adrienne Anginot, Georges Uzan

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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
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  9. Article
  10. Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Article
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  15. Article
  16. Adipokines in atherosclerosis: unraveling complex roles.Frontiers in cardiovascular medicine · 2023
    Review
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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

8 authors at 2 institutions in 1 country.

Guillaume HaINSERM U1197, Hôpital Paul Brousse, Villejuif, France.ORCID 0000-0002-4942-378X
Fanny De TorresINSERM U1197, Hôpital Paul Brousse, Villejuif, France.
Nassim AroucheINSERM U1197, Hôpital Paul Brousse, Villejuif, France.
Nassima BenzoubirUMRS-1193, Hôpital Paul Brousse, Villejuif, France.
Ségolène FerratgeCellenion, Hôpital Paul Brousse, Villejuif, France.
Elie HatemINSERM U1197, Hôpital Paul Brousse, Villejuif, France.
Adrienne AnginotINSERM U1197, Hôpital Paul Brousse, Villejuif, France.
Georges UzanINSERM U1197, Hôpital Paul Brousse, Villejuif, France.
Inserm · FRHôpital Paul-Brousse · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction (ED) is part of the first steps in the development of cardiovascular diseases (CVD). Growth Differentiation Factor 15 (GDF15) is a cytokine belonging to the Transforming Growth Factor β superfamily and its expression is increased both during ED and in CVD. Because high blood levels of GDF15 have been reported during ED, we hypothesized that GDF15 could be produced by endothelial cells in response to a vascular stress, possibly to attenuate endothelial function loss. Since senescence is mainly involved in both vascular stress and endothelial function loss, we used Endothelial Colony Forming Cells generated from adult blood (AB-ECFCs) as a model of endothelial cells to investigate GDF15 expression during cellular senescence. Then, we analyzed the potential role of GDF15 in AB-ECFC functions and senescence. When AB-ECFCs become senescent, they secrete increased levels of GDF15. We investigated GDF15 paracrine effects on non-senescent AB-ECFCs and showed that GDF15 enhanced proliferation, migration, NO production and activated several signaling pathways including AKT, ERK1/2 and SMAD2 without triggering any oxidative stress. Taken together, our results suggest that GDF15 production by senescent AB-ECFCs could act in a paracrine manner on non-senescent AB-ECFCs, and that this interaction could be beneficial to its model cells. Therefore, GDF15 could play a beneficial role in a dysfunctional vascular system as previously reported in patients with CVD, by limiting ED related to vascular stress occurring in these diseases.

Indexed as

AdultAgedBlood CellsCell MovementCell ProliferationCell SurvivalCellular SenescenceEndothelial CellsGrowth Differentiation Factor 15HumansMaleMiddle AgedNitric OxideOxidative StressSignal TransductionUp-RegulationGDF15 protein, humanGrowth Differentiation Factor 15Nitric Oxide

Identifiers

PMID31075112
PMCPMC6510423
OpenAlexW2943985492

What OpenQuestion 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 OpenQuestion graph.