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Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth

Author

Listed:
  • L. M. Schiffmann

    (University of Cologne
    University of Cologne
    Centre for Integrated Oncology (CIO) Cologne Bonn)

  • J. P. Werthenbach

    (University of Cologne)

  • F. Heintges-Kleinhofer

    (University of Cologne)

  • J. M. Seeger

    (University of Cologne)

  • M. Fritsch

    (University of Cologne)

  • S. D. Günther

    (University of Cologne)

  • S. Willenborg

    (University of Cologne
    University of Cologne)

  • S. Brodesser

    (University of Cologne)

  • C. Lucas

    (University of Cologne)

  • C. Jüngst

    (University of Cologne)

  • M. C. Albert

    (University of Cologne)

  • F. Schorn

    (University of Cologne)

  • A. Witt

    (University of Cologne)

  • C. T. Moraes

    (University of Miami)

  • C. J. Bruns

    (University of Cologne
    Centre for Integrated Oncology (CIO) Cologne Bonn)

  • M. Pasparakis

    (University of Cologne)

  • M. Krönke

    (University of Cologne)

  • S. A. Eming

    (University of Cologne
    University of Cologne)

  • O. Coutelle

    (University of Cologne)

  • H. Kashkar

    (University of Cologne
    University of Cologne)

Abstract

The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we assess the impact of mitochondrial bioenergetics on neovascularisation, by deleting cox10 gene encoding an assembly factor of cytochrome c oxidase (COX) specifically in mouse ECs, providing a model for vasculature-restricted respiratory deficiency. We show that EC-specific cox10 ablation results in deficient vascular development causing embryonic lethality. In adult mice induction of EC-specific cox10 gene deletion produces no overt phenotype. However, the angiogenic capacity of COX-deficient ECs is severely compromised under energetically demanding conditions, as revealed by significantly delayed wound-healing and impaired tumour growth. We provide genetic evidence for a requirement of mitochondrial respiration in vascular endothelial cells for neoangiogenesis during development, tissue repair and cancer.

Suggested Citation

  • L. M. Schiffmann & J. P. Werthenbach & F. Heintges-Kleinhofer & J. M. Seeger & M. Fritsch & S. D. Günther & S. Willenborg & S. Brodesser & C. Lucas & C. Jüngst & M. C. Albert & F. Schorn & A. Witt & C, 2020. "Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth," Nature Communications, Nature, vol. 11(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17472-2
    DOI: 10.1038/s41467-020-17472-2
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    Cited by:

    1. Haifeng Zhang & Busu Li & Qunhua Huang & Francesc López-Giráldez & Yoshiaki Tanaka & Qun Lin & Sameet Mehta & Guilin Wang & Morven Graham & Xinran Liu & In-Hyun Park & Anne Eichmann & Wang Min & Jenny, 2022. "Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas," Nature Communications, Nature, vol. 13(1), pages 1-21, December.

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