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Neonatal hyperoxia inhibits proliferation of atrial cardiomyocytes by suppressing fatty acid synthesis

Ethan David Cohen, Min Yee, George A. Porter Jr., Andrew N. McDavid, View ORCID ProfilePaul S. Brookes, Gloria S. Pryhuber, Michael A. O’Reilly
doi: https://doi.org/10.1101/2020.06.01.127621
Ethan David Cohen
1The Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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  • For correspondence: Ethan_Cohen@urmc.rochester.edu michael_oreilly@urmc.rochester.edu
Min Yee
1The Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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George A. Porter Jr.
1The Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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Andrew N. McDavid
2The Department of Biostatistics & Computational Biology, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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Paul S. Brookes
3The Department of Anesthesiology, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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Gloria S. Pryhuber
1The Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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Michael A. O’Reilly
1The Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642
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  • For correspondence: Ethan_Cohen@urmc.rochester.edu michael_oreilly@urmc.rochester.edu
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ABSTRACT

Preterm birth increases the risk for pulmonary hypertension and heart failure in adulthood. Oxygen therapy can damage the immature cardiopulmonary system and may be partially responsible for the cardiovascular disease in adults born preterm. We previously showed that exposing newborn mice to hyperoxia causes pulmonary hypertension by 1 year of age that is preceded by a poorly understood loss of pulmonary vein cardiomyocyte proliferation. We now show that hyperoxia also inhibits the proliferation of left atrial cardiomyocytes and causes diastolic heart failure by thinning the walls of the left atrium and disrupting its ability to pump effectively. Transcriptomic profiling showed that neonatal hyperoxia permanently suppressed fatty acid synthase (Fasn), stearoyl-CoA desaturase 1 (Scd1) and other fatty acid synthesis genes in the atria of mice, the HL-1 line of mouse atrial cardiomyocytes and left atrial tissue explanted from human infants. Suppressing Fasn or Scd1 reduced HL-1 cell proliferation while overexpressing these genes maintained their expansion in hyperoxic conditions, suggesting hyperoxia directly inhibits atrial cardiomyocyte proliferation by repressing Fasn and Scd1. Pharmacologic interventions that restore Fasn, Scd1 and other fatty acid synthesis genes in atrial cardiomyocytes may thus provide a way of ameliorating the adverse effects of supplemental oxygen on preterm infants.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted June 02, 2020.
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Neonatal hyperoxia inhibits proliferation of atrial cardiomyocytes by suppressing fatty acid synthesis
Ethan David Cohen, Min Yee, George A. Porter Jr., Andrew N. McDavid, Paul S. Brookes, Gloria S. Pryhuber, Michael A. O’Reilly
bioRxiv 2020.06.01.127621; doi: https://doi.org/10.1101/2020.06.01.127621
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Neonatal hyperoxia inhibits proliferation of atrial cardiomyocytes by suppressing fatty acid synthesis
Ethan David Cohen, Min Yee, George A. Porter Jr., Andrew N. McDavid, Paul S. Brookes, Gloria S. Pryhuber, Michael A. O’Reilly
bioRxiv 2020.06.01.127621; doi: https://doi.org/10.1101/2020.06.01.127621

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