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Uncontrolled angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1

Author

Listed:
  • Yidong Wang

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Bingruo Wu

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Pengfei Lu

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Donghong Zhang

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Brian Wu

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Shweta Varshney

    (Albert Einstein College of Medicine)

  • Gonzalo Monte-Nieto

    (Victor Chang Cardiac Research Institute
    St. Vincent’s Clinical School, University of New South Wales)

  • Zhenwu Zhuang

    (Yale University)

  • Rabab Charafeddine

    (Albert Einstein College of Medicine)

  • Adam H. Kramer

    (Albert Einstein College of Medicine)

  • Nicolas E. Sibinga

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Nikolaos G. Frangogiannis

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Richard N. Kitsis

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Ralf H. Adams

    (Max-Planck-Institute for Molecular Biomedicine)

  • Kari Alitalo

    (Wihuri Research Institute, Biomedicum Helsinki)

  • David J. Sharp

    (Albert Einstein College of Medicine)

  • Richard P. Harvey

    (Victor Chang Cardiac Research Institute
    St. Vincent’s Clinical School, University of New South Wales
    University of New South Wales)

  • Pamela Stanley

    (Albert Einstein College of Medicine)

  • Bin Zhou

    (Wilf Cardiovascular Research Institute, Albert Einstein College of Medicine
    The First Affiliated Hospital of Nanjing Medical University)

Abstract

Coronary artery anomalies may cause life-threatening cardiac complications; however, developmental mechanisms underpinning coronary artery formation remain ill-defined. Here we identify an angiogenic cell population for coronary artery formation in mice. Regulated by a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis, these angiogenic cells generate mature coronary arteries. The NOTCH modulator POFUT1 critically regulates this signaling axis. POFUT1 inactivation disrupts signaling events and results in excessive angiogenic cell proliferation and plexus formation, leading to anomalous coronary arteries, myocardial infarction and heart failure. Simultaneous VEGFR2 inactivation fully rescues these defects. These findings show that dysregulated angiogenic precursors link coronary anomalies to ischemic heart disease.

Suggested Citation

  • Yidong Wang & Bingruo Wu & Pengfei Lu & Donghong Zhang & Brian Wu & Shweta Varshney & Gonzalo Monte-Nieto & Zhenwu Zhuang & Rabab Charafeddine & Adam H. Kramer & Nicolas E. Sibinga & Nikolaos G. Frang, 2017. "Uncontrolled angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00654-w
    DOI: 10.1038/s41467-017-00654-w
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    Cited by:

    1. Pengfei Lu & Ping Wang & Bingruo Wu & Yidong Wang & Yang Liu & Wei Cheng & Xuhui Feng & Xinchun Yuan & Miriam M. Atteya & Haleigh Ferro & Yukiko Sugi & Grant Rydquist & Mahdi Esmaily & Jonathan T. But, 2022. "A SOX17-PDGFB signaling axis regulates aortic root development," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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