Identification of a hybrid myocardial zone in the mammalian heart after birth

Xueying Tian, Yan Li, Lingjuan He, Hui Zhang, Xiuzhen Huang, Qiaozhen Liu, Wenjuan Pu, Libo Zhang, Yi Li, Huan Zhao, Zhifu Wang, Jianhong Zhu, Yu Nie, Shengshou Hu, David Sedmera, Tao P. Zhong, Ying Yu, Li Zhang, Yan Yan, Zengyong Qiao, Qing-Dong Wang, Sean M. Wu, William T. Pu, Robert H. Anderson and Bin Zhou ()
Additional contact information
Xueying Tian: University of Chinese Academy of Sciences
Yan Li: University of Chinese Academy of Sciences
Lingjuan He: University of Chinese Academy of Sciences
Hui Zhang: University of Chinese Academy of Sciences
Xiuzhen Huang: University of Chinese Academy of Sciences
Qiaozhen Liu: University of Chinese Academy of Sciences
Wenjuan Pu: University of Chinese Academy of Sciences
Libo Zhang: University of Chinese Academy of Sciences
Yi Li: University of Chinese Academy of Sciences
Huan Zhao: University of Chinese Academy of Sciences
Zhifu Wang: Fudan University
Jianhong Zhu: Fudan University
Yu Nie: Chinese Academy of Medical Sciences and Peking Union Medical College
Shengshou Hu: Chinese Academy of Medical Sciences and Peking Union Medical College
David Sedmera: Charles University; Institute of Physiology The Czech Academy of Sciences
Tao P. Zhong: Fudan University
Ying Yu: University of Chinese Academy of Sciences
Li Zhang: Zhejiang University
Yan Yan: Fudan University
Zengyong Qiao: Southern Medical University Affiliated Fengxian Hospital
Qing-Dong Wang: Innovative Medicines and Early Clinical Development Biotech Unit, AstraZeneca
Sean M. Wu: Stanford University School of Medicine
William T. Pu: Harvard University
Robert H. Anderson: Newcastle University
Bin Zhou: University of Chinese Academy of Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Noncompaction cardiomyopathy is characterized by the presence of extensive trabeculations, which could lead to heart failure and malignant arrhythmias. How trabeculations resolve to form compact myocardium is poorly understood. Elucidation of this process is critical to understanding the pathophysiology of noncompaction disease. Here we use genetic lineage tracing to mark the Nppa+ or Hey2+ cardiomyocytes as trabecular and compact components of the ventricular wall. We find that Nppa+ and Hey2+ cardiomyocytes, respectively, from the endocardial and epicardial zones of the ventricular wall postnatally. Interposed between these two postnatal layers is a hybrid zone, which is composed of cells derived from both the Nppa+ and Hey2+ populations. Inhibition of the fetal Hey2+ cell contribution to the hybrid zone results in persistence of excessive trabeculations in postnatal heart. Our findings indicate that the expansion of Hey2+ fetal compact component, and its contribution to the hybrid myocardial zone, are essential for normal formation of the ventricular walls.

Date: 2017
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DOI: 10.1038/s41467-017-00118-1

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