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Gladstone scientists identify genetic mechanism linked to congenital heart disease
Date:1/22/2012

genes must remain off to ensure the development of a healthy heart.

In laboratory experiments, Drs. Bruneau and Delgado-Olguin removed Ezh2 from mice at various developmental stages, monitoring any ensuing genetic or physical changes and comparing them to mice whose Ezh2 remained intact. Surprisingly, mice without Ezh2 developed normally in the uterus. It wasn't until after birth that they began to show problems. Their hearts became enlarged and weakened and were unable to pump blood efficiently. An enlarged heart is a hallmark feature of cardiomyopathy, a form of congenital heart disease that afflicts thousands of children each year and for which the only manifestation may be sudden death.

Further analysis revealed that Six1 is normally on only for a brief period during heart development, after which Ezh2 shuts it off for good. But without Ezh2 to act as a regulator, Six1 remains onleading to heart problems later in life.

"When Six1 remains active for too long in Ezh2-deficient mice, it boosts the activity of other genes that shouldn't be activated in heart-muscle cellssuch as genes that make skeletal muscle," said Dr. Delgado-Olguin. "The enlargement and thickening of the mice's hearts over time eventually led to heart failure."

This breakthrough may help researchers improve their understanding of the genetic causes of congenital heart disease while also pointing the way to potential therapies. For example, a type of congenital heart disease called dilated cardiomyopathy is caused by mutations in Eya4, a gene that is also regulated by Ezh2 in the heart.

"Six1 is just one of many Ezh2-regulated genes that are vital for heart development," said Dr. Bruneau. "Our next goal is to find out exactly how Ezh2 regulates these other genes, so that we can begin to develop a complete genomic blueprint of how a heart becomes a heart."


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Contact: Anne Holden
anne.holden@gladstone.ucsf.edu
415-734-2534
Gladstone Institutes
Source:Eurekalert  

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