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Opposite effects of Activin type 2 receptor ligands on cardiomyocyte proliferation during development and repair

Author

Listed:
  • Deepika Dogra

    (Max Planck Institute for Heart and Lung Research)

  • Suchit Ahuja

    (Max Planck Institute for Heart and Lung Research)

  • Hyun-Taek Kim

    (Max Planck Institute for Heart and Lung Research)

  • S. Javad Rasouli

    (Max Planck Institute for Heart and Lung Research)

  • Didier Y. R. Stainier

    (Max Planck Institute for Heart and Lung Research
    University of California San Francisco)

  • Sven Reischauer

    (Max Planck Institute for Heart and Lung Research
    University of California San Francisco)

Abstract

Zebrafish regenerate damaged myocardial tissue very effectively. Hence, insights into the molecular networks underlying zebrafish heart regeneration might help develop alternative strategies to restore human cardiac performance. While TGF-β signaling has been implicated in zebrafish cardiac regeneration, the role of its individual ligands remains unclear. Here, we report the opposing expression response during zebrafish heart regeneration of two genes, mstnb and inhbaa, which encode TGF-β family ligands. Using gain-of-function (GOF) and loss-of-function (LOF) approaches, we show that these ligands mediate inverse effects on cardiac regeneration and specifically on cardiomyocyte (CM) proliferation. Notably, we find that Inhbaa functions as a CM mitogen and that its overexpression leads to accelerated cardiac recovery and scar clearance after injury. In contrast, mstnb GOF and inhbaa LOF both lead to unresolved scarring after cardiac injury. We further show that Mstnb and Inhbaa inversely control Smad2 and Smad3 transcription factor activities through alternate Activin type 2 receptors.

Suggested Citation

  • Deepika Dogra & Suchit Ahuja & Hyun-Taek Kim & S. Javad Rasouli & Didier Y. R. Stainier & Sven Reischauer, 2017. "Opposite effects of Activin type 2 receptor ligands on cardiomyocyte proliferation during development and repair," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01950-1
    DOI: 10.1038/s41467-017-01950-1
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