Endothelial deletion of Ino80 disrupts coronary angiogenesis and causes congenital heart disease

Siyeon Rhee, Jae I. Chung, Devin A. King, Gaetano D’amato, David T. Paik, Anna Duan, Andrew Chang, Danielle Nagelberg, Bikram Sharma, Youngtae Jeong, Maximilian Diehn, Joseph C. Wu, Ashby J. Morrison () and Kristy Red-Horse ()
Additional contact information
Siyeon Rhee: Stanford University
Jae I. Chung: Stanford University
Devin A. King: Stanford University
Gaetano D’amato: Stanford University
David T. Paik: Stanford University School of Medicine
Anna Duan: Stanford University
Andrew Chang: Stanford University
Danielle Nagelberg: Stanford University
Bikram Sharma: Stanford University
Youngtae Jeong: Stanford University School of Medicine
Maximilian Diehn: Stanford University School of Medicine
Joseph C. Wu: Stanford University School of Medicine
Ashby J. Morrison: Stanford University
Kristy Red-Horse: Stanford University

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract During development, the formation of a mature, well-functioning heart requires transformation of the ventricular wall from a loose trabecular network into a dense compact myocardium at mid-gestation. Failure to compact is associated in humans with congenital diseases such as left ventricular non-compaction (LVNC). The mechanisms regulating myocardial compaction are however still poorly understood. Here, we show that deletion of the Ino80 chromatin remodeler in vascular endothelial cells prevents ventricular compaction in the developing mouse heart. This correlates with defective coronary vascularization, and specific deletion of Ino80 in the two major coronary progenitor tissues—sinus venosus and endocardium—causes intermediate phenotypes. In vitro, endothelial cells promote myocardial expansion independently of blood flow in an Ino80-dependent manner. Ino80 deletion increases the expression of E2F-activated genes and endothelial cell S-phase occupancy. Thus, Ino80 is essential for coronary angiogenesis and allows coronary vessels to support proper compaction of the heart wall.

Date: 2018
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DOI: 10.1038/s41467-017-02796-3

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