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Regulatory pathways governing murine coronary vessel formation are dysregulated in the injured adult heart

Author

Listed:
  • Sophie Payne

    (University of Oxford
    University of Oxford)

  • Mala Gunadasa-Rohling

    (University of Oxford)

  • Alice Neal

    (University of Oxford
    University of Oxford)

  • Andia N. Redpath

    (University of Oxford)

  • Jyoti Patel

    (University of Oxford, John Radcliffe Hospital)

  • Kira M. Chouliaras

    (University of Oxford)

  • Indrika Ratnayaka

    (University of Oxford)

  • Nicola Smart

    (University of Oxford)

  • Sarah De Val

    (University of Oxford
    University of Oxford)

Abstract

The survival of ischaemic cardiomyocytes after myocardial infarction (MI) depends on the formation of new blood vessels. However, endogenous neovascularization is inefficient and the regulatory pathways directing coronary vessel growth are not well understood. Here we describe three independent regulatory pathways active in coronary vessels during development through analysis of the expression patterns of differentially regulated endothelial enhancers in the heart. The angiogenic VEGFA-MEF2 regulatory pathway is predominantly active in endocardial-derived vessels, whilst SOXF/RBPJ and BMP-SMAD pathways are seen in sinus venosus-derived arterial and venous coronaries, respectively. Although all developmental pathways contribute to post-MI vessel growth in the neonate, none are active during neovascularization after MI in adult hearts. This was particularly notable for the angiogenic VEGFA-MEF2 pathway, otherwise active in adult hearts and during neoangiogenesis in other adult settings. Our results therefore demonstrate a fundamental divergence between the regulation of coronary vessel growth in healthy and ischemic adult hearts.

Suggested Citation

  • Sophie Payne & Mala Gunadasa-Rohling & Alice Neal & Andia N. Redpath & Jyoti Patel & Kira M. Chouliaras & Indrika Ratnayaka & Nicola Smart & Sarah De Val, 2019. "Regulatory pathways governing murine coronary vessel formation are dysregulated in the injured adult heart," Nature Communications, Nature, vol. 10(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10710-2
    DOI: 10.1038/s41467-019-10710-2
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