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NKX2-5 regulates human cardiomyogenesis via a HEY2 dependent transcriptional network

David J Anderson1, David I Kaplan2, Katrina M Bell1

  • 1Murdoch Childrens Research Institute, Royal Children's Hospital, Flemington Road, Parkville, VIC, 3052, Australia.

Nature Communications
|April 12, 2018
PubMed

Insights

Deleting NKX2-5 in human embryonic stem cells impairs heart cell development and function. The bHLH protein HEY2 mediates NKX2-5

Area of Science:

  • Developmental Biology
  • Stem Cell Biology
  • Cardiovascular Research

Background:

  • Congenital heart defects arise from genetic mutations affecting cardiac lineage formation.
  • NKX2-5 is a crucial gene in the cardiac gene regulatory network.

Purpose of the Study:

  • To investigate the role of NKX2-5 in human cardiomyogenesis using human embryonic stem cells (hESCs).
  • To identify downstream targets and mediators of NKX2-5 function in heart development.

Main Methods:

  • Gene deletion of NKX2-5 in hESCs.
  • Analysis of cardiomyogenesis, cell surface markers (VCAM1, PDGFRα), and cardiomyocyte physiology.
  • Molecular profiling and genetic rescue experiments.

Main Results:

  • NKX2-5 deletion led to impaired cardiomyogenesis and abnormal cell marker expression.
  • NKX2-5 null cardiomyocytes exhibited asynchronous contractions and altered action potentials.
  • HEY2 was identified as a key mediator of NKX2-5 function.

Conclusions:

  • HEY2 is a novel component of the NKX2-5 cardiac transcriptional network.
  • hESC models are valuable for studying human heart development and congenital heart disease.
  • This study provides a human context for evaluating pathogenic mutations in congenital heart disease.

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