Congenital heart defects are the most common type of birth defect,
affecting 35,000 babies in the United States each year, estimates the
U.S. Department of Health and Human Services.
Many of these defects
originate as the heart chambers are forming. While much is known about
the development of the heart, the formation of the four distinct
chambers of the heart has lacked thorough understanding.
‘A population of progenitor cells expressing protein-coding gene Foxa2 during early development gives rise to cardiovascular cells of both the left and right ventricular chambers, but not the atria.’
An in-depth understanding of the formation of the heart chambers
will enable us to better comprehend the biology behind detrimental heart
defects and how best to address them.
A population of cells in early development may give rise to the
ventricular chambers of the heart, but not the atria, revealed a
study led by researchers from the Mindich Child Health and Development
Institute at the Icahn School of Medicine at Mount Sinai and published
today in Nature Communications
Using a model that traces cell lineage in mice, investigators
studied the protein-coding gene Foxa2, primarily associated with
endoderm and ectoderm development during embryogenesis. They discovered
a population of progenitor cells expressing Foxa2 during early
development that gave rise to cardiovascular cells of both the left and
right ventricular chambers, but not the atria. Their research showed
that atrial-ventricular segregation may occur long before the
morphological establishment of differentiated cardiac structures.
Lead investigator Nicole
Dubois, Assistant Professor in the Department of Cell,
Developmental and Regenerative Biology at the Icahn School of Medicine
at Mount Sinai, said, "In addition to informing our understanding of early
heart development, we hope that these findings will also lead to new
protocols for the generation of ventricular cardiomyocytes in cell
culture that could potentially be used in therapeutic settings."
"There is a lot we still don't understand about this population, or
the function of Foxa2 during the formation of the heart, but we think
these findings provide a powerful new system to answer some of the most
relevant open questions about how early heart development occurs," said
Evan Bardot, PhD student and first author of the Nature Communications