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UCSD finds genetic time bomb in heart that leads to heart failure in some patients

logist and one of the authors of the paper in Cell. "Then, over a period of several years, they developed problems with the conduction system the electrical system in the heart."

Silberbach and another co-author, Siew Yen Ho, Ph.D., were able to compare the human-patient results with the studies in mice by Chien and his team. The UCSD mice, which were created without Nkx2-5 in specific compartments of the heart, were shown to have significant deterioration of their AV nodes. This included an under-formed AV node and disorganized cellular tissue, as compared to normal mice. Similar AV node deterioration was seen in the human patients. Also similar in both mice and humans was a progressive, massive overgrowth of cardiac muscle as they aged.

"With these studies, we learned that Nkx2-5 is critical not only for heart formation, but also for maintenance of heart function," Chien said. "It also showed us that our mouse model closely resembled the human disease and therefore was an ideal experimental animal model for studies of this form of congenital heart disease caused by the Nkx2-5 mutation."

To determine what was causing the excessive overgrowth in the hearts of Nkx2-5-deficient humans and mice, the UCSD researchers began a search for genes changed by the deficiency. They utilized DNA microarrays, which track the expression the turning on and off of thousands of genes in a single, high-speed test, and used computer technology to compare the results to large 30,000 gene databases that were generated from multiple other forms of heart muscle disease. What they found was a growth-factor gene called BMP-10 that was expressed 500 times higher in Nkx2-5-deficient mice, as compared to normal mice, and the gene was unique to this specific form of congenital heart disease. Normally, BMP-10 is only active during fetal heart development, not later in life.

The team
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Contact: Sue Pondrom
spondrom@ucsd.edu
619-543-6163
University of California - San Diego
29-Apr-2004


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