logomark
Research

Research

BDR researchers coming from diverse research fields are working together to achieve higher goals.

Seminars & Symposia

Seminars & Symposia

BDR hosts annual symposium and regular seminars inviting international scientists in life science.

Careers & Study

Careers & Study

BDR embraces people from diverse backgrounds, and strives to create an open and supportive setting for research.

Outreach

Outreach

BDR communicates the appeal and significance of our research to society through the use of various media and activities.

News

News

From research, events, people and everything in between, find out what’s going on at RIKEN BDR.

About Us

About Us

Exploring the scientific foundations of life through interdisciplinary approaches to address society’s problems.

Modelling cardiac chamber development in iPS cells and mice
May 14, 2018 13:30 - 15:00

Category

Seminar

Place

Kobe

Venue

DB Bldg. Auditorium C1F

Speaker

Richard P. Harvey

Affiliation

Victor Chang Cardiac Research Institute

Summary

Central to heart patterning during development is the division of the forming heart tube into chamber and non-chamber myocardium. The pumping chambers (ventricles) develop a luminal sponge-like network of cardiomyocytes (CMs) called trabeculae, which drive chamber growth and constitute the force-generating and conduction components of the early heart. Trabeculae also contribute to ventricular septation, papillary muscles, conduction tracts, and wall thickening through a process called compaction. Thus, trabeculation is critical to many aspects of heart morphogenesis and has likely provided a flexible evolutionary template for heart evolution. In animal models, defective trabeculation leads to embryonic lethality, while in humans, defective chamber growth and trabeculation can lead to severe congenital conditions including hypoplastic left heart (HLH) and non-compaction cardiomyopathy. I will touch on two studies. In the first, we are modelling the genetic and network basis of HLH in human IPS cells. Here, we hypothesize that HLH occurs at the intersection of hemodynamic changes brought about by defects in valves and outflow vessels, and a fundamental deficit in ventricular myocyte growth and function. In a second study, we have developed an entirely new model of cardiac trabeculation in which we propose that antagonistic interactions between the NOTCH and NEUREGULIN (NRG) signaling pathways control endocardial and myocardial behaviors, and the dynamic synthesis and degradation of cardiac extracellular matrix to define the basic segmental units of chamber sub-structure.

Host

Hiroshi Hamada

PAGE
TOP