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FOXF1 Mediates Endothelial Progenitor Functions and Regulates Vascular Sprouting.
Caterina Sturtzel1, Karoline Lipnik1, Renate Hofer-Warbinek1
1Department of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Frontiers in Bioengineering and Biotechnology
|July 3, 2018
Summary
The forkhead box transcription factor FOXF1 is crucial for endothelial progenitor cells, promoting vascular sprouting by regulating Notch2 and VEGF receptor-2. This finding is vital for understanding neovascularization and tissue repair.
Area of Science:
- Vascular Biology
- Cell Biology
- Developmental Biology
Background:
- Endothelial colony-forming cells (ECFCs) are crucial for neovascularization.
- Identifying key regulators of ECFC progenitor status is essential for understanding vascular development.
Purpose of the Study:
- To investigate the role of the forkhead box transcription factor FOXF1 in endothelial progenitor cells.
- To elucidate the molecular mechanisms by which FOXF1 influences vascular sprouting and neovascularization.
Main Methods:
- Gain- and loss-of-function studies in human ECFCs.
- Analysis of gene expression, including Notch2, VEGF receptor-2, ephrin B2, and EphB4.
- In vivo studies using a zebrafish model of embryonic vascular development.
Main Results:
- FOXF1 is selectively expressed in ECFCs compared to mature endothelial cells.
- FOXF1 overexpression enhances ECFC sprouting capacity, while its knockdown reduces it.
- FOXF1 regulates the expression of Notch2, VEGF receptor-2, ephrin B2, and EphB4, impacting vascular sprouting in both human cells and zebrafish embryos.
Conclusions:
- FOXF1 plays a critical role in endothelial progenitor cell function and vascular sprouting.
- FOXF1's downstream mediators include Notch2, VEGF receptor-2, and ephrin B2, highlighting its significance in neovascularization.
- Targeting FOXF1 may offer therapeutic potential for promoting tissue neovascularization.
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