Hif-1α regulates macrophage-endothelial interactions during blood vessel development in zebrafish

Claudia Gerri, Rubén Marín-Juez, Michele Marass, Alora Marks, Hans-Martin Maischein and Didier Y R. Stainier ()
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Claudia Gerri: Max Planck Institute for Heart and Lung Research
Rubén Marín-Juez: Max Planck Institute for Heart and Lung Research
Michele Marass: Max Planck Institute for Heart and Lung Research
Alora Marks: Max Planck Institute for Heart and Lung Research
Hans-Martin Maischein: Max Planck Institute for Heart and Lung Research
Didier Y R. Stainier: Max Planck Institute for Heart and Lung Research

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Macrophages are known to interact with endothelial cells during developmental and pathological angiogenesis but the molecular mechanisms modulating these interactions remain unclear. Here, we show a role for the Hif-1α transcription factor in this cellular communication. We generated hif-1aa;hif-1ab double mutants in zebrafish, hereafter referred to as hif-1α mutants, and find that they exhibit impaired macrophage mobilization from the aorta-gonad-mesonephros (AGM) region as well as angiogenic defects and defective vascular repair. Importantly, macrophage ablation is sufficient to recapitulate the vascular phenotypes observed in hif-1α mutants, revealing for the first time a macrophage-dependent angiogenic process during development. Further substantiating our observations of vascular repair, we find that most macrophages closely associated with ruptured blood vessels are Tnfα-positive, a key feature of classically activated macrophages. Altogether, our data provide genetic evidence that Hif-1α regulates interactions between macrophages and endothelial cells starting with the mobilization of macrophages from the AGM.

Date: 2017
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DOI: 10.1038/ncomms15492

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