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Injection Reverses Heart-Attack Damage
Date:7/23/2009

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When the researchers also stimulated production of a cellular receptor for NRG1, known as ErbB4, cardiomyocyte proliferation was further enhanced, demonstrating that NRG1 works by stimulating this receptor. They also identified the specific kinds of cardiomyocytes (mononucleated) that are most likely to respond to treatment.

In 2007, Kuhn and colleagues first demonstrated that the heart has dormant regenerative capacities that can be reawakened. Kuhn developed a sponge-like patch, soaked in a compound called periostin that is abundant in the developing fetal heart (and in injured skeletal muscle) but scarce in adult hearts. When the patch was placed over the site of cardiac injury in rats, it induced cardiomyocyte proliferation and improved heart function (Nature Medicine 2007; 13:962-9). Similar results were seen in larger animals, and periostin is now in preclinical development at Children's Hospital Boston for future application in human patients with heart failure.

The new work adds a second compound to the heart-regeneration toolbox, and reveals how both periostin and NRG1 work at the cellular and molecular level, an essential step in predicting possible side effects. Both compounds ultimately act on the same cellular pathway, Kuhn found.

"We applied periostin locally at the site of cardiac injury, but NRG1 works when given by systemic injection - a very promising result that suggests it may be feasible to use this in the clinic to treat heart failure," says Kuhn, who won a first prize Young Investigator Award, from the American College of Cardiology in 2007.

The study was funded by the Department of Cardiology at Children's Hospital Boston, the Charles Hood Foundation, and the American Heart Association.

Children's Hospital Boston is home to the world's largest research enterprise
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SOURCE Children's Hospital of Boston
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