Evidence map›Paper›PMID 29963552›Full record

ArticleFrontiers in bioengineering and biotechnology2018

FOXF1 Mediates Endothelial Progenitor Functions and Regulates Vascular Sprouting.

Caterina Sturtzel, Karoline Lipnik, Renate Hofer-Warbinek, Julia Testori, Bettina Ebner, Jaqueline Seigner, Ping Qiu, Martin Bilban, Anita Jandrositz, Karl-Heinz Preisegger and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in bioengineering and biotechnology, 2018. 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
1.0field-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, 27 citations in OpenAlex.

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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

15 authors at 3 institutions in 2 countries.

Caterina SturtzelDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Karoline LipnikDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Renate Hofer-WarbinekDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Julia TestoriDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Bettina EbnerDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Jaqueline SeignerDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Ping QiuDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Martin BilbanDepartment of Laboratory Medicine & Core Facility Genomics, Core Facilities, Medical University of Vienna, Vienna, Austria.
Anita JandrositzVivoCell Biosolutions GmbH, Graz, Austria.
Karl-Heinz PreiseggerVivoCell Biosolutions GmbH, Graz, Austria.
Gerold UntergasserLaboratory for Tumor Biology & Angiogenesis, Medical University of Innsbruck, Innsbruck, Austria.
Eberhard GunsiliusLaboratory for Tumor Biology & Angiogenesis, Medical University of Innsbruck, Innsbruck, Austria.
Rainer de MartinDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Jens KrollDepartment of Vascular Biology and Tumor Angiogenesis, European for Center for Angioscience, Medical Faculty Mannheim of Heidelberg University, Mannheim, Germany.
Erhard HoferDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATInnsbruck Medical University · ATHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial colony forming cells (ECFC) or late blood outgrowth endothelial cells (BOEC) have been proposed to contribute to neovascularization in humans. Exploring genes characteristic for the progenitor status of ECFC we have identified the forkhead box transcription factor FOXF1 to be selectively expressed in ECFC compared to mature endothelial cells isolated from the vessel wall. Analyzing the role of FOXF1 by gain- and loss-of-function studies we detected a strong impact of FOXF1 expression on the particularly high sprouting capabilities of endothelial progenitors. This apparently relates to the regulation of expression of several surface receptors. First, FOXF1 overexpression specifically induces the expression of Notch2 receptors and induces sprouting. Vice versa, knock-down of FOXF1 and Notch2 reduces sprouting. In addition, FOXF1 augments the expression of VEGF receptor-2 and of the arterial marker ephrin B2, whereas it downmodulates the venous marker EphB4. In line with these findings on human endothelial progenitors, we further show that knockdown of FOXF1 in the zebrafish model alters, during embryonic development, the regular formation of vasculature by sprouting. Hence, these findings support a crucial role of FOXF1 for endothelial progenitors and connected vascular sprouting as it may be relevant for tissue neovascularization. It further implicates Notch2, VEGF receptor-2, and ephrin B2 as downstream mediators of FOXF1 functions.

Indexed as

ECFCendothelial progenitorsephrinB2FOXF1intersegmental capillariesNotch2vascular sprouting

Identifiers

PMID29963552
PMCPMC6010557
OpenAlexW2804710466

What OpenQuestion holds

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Registered trials

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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.