This week, Srivastava, who holds the Pogue Distinguished Chair in Research on Cardiac Birth Defects, reports that a protein the heart produces during its development could be redeployed after a heart attack to help the organ repair itself.

The mouse-study findings could eventually lead to new treatments for heart disease in humans and could even change the way healthcare providers respond to people who suffer from heart attacks. The research appears in today’s edition of Nature and is available online.

“If the protein has a similar effect in humans as it does in mice, the impact by sheer volume is great – nearly 1 million people have heart attacks every year just in the United States,” said Srivastava, the study’s senior author. “The delivery is very simple and avoids many of the problems of using stem cells.”

While more common in adults, heart disease is the leading noninfectious cause of death in children younger than one year. Heart disease in children is usually caused by developmental abnormalities.

Embryos express the protein, Thymosin beta-4, during the heart’s development. It encourages the migration of heart cells and affects those cells’ survivability. The new findings show that the protein prevents cell death after an experimentally induced heart attack and limits the degree of scar tissue formation.

Thymosin beta-4 is already used in clinical trials to promote wound healing on the skin. As a result, the protein could enter clinical trials for treating the heart in the very near future, said Srivastava, co-director of the March of Dimes Birth Defects Center at UT Southwestern.

During their study, UT Southwestern researchers discovered that Thymosin beta-4 works in conjunction with two other proteins to promote survival and migration of heart muscle cells by activating the protein Akt/Protein Kinase B. Akt/PKB, which promotes cell survival.

After studying the activity of cells in culture, researchers created a mouse model by tying off the coronary artery of 58 adult mice, simulating a heart attack. Half of the mice were given Thymosin beta-4 systemically, directly into the heart, or through both routes immediately after the ligation. The other half was given control injections of saline immediately after the artery was tied off.

Researchers found that Thymosin beta-4 caused fewer cells in the affected part of the heart to die, resulting in improved function even several weeks after the heart attack. Researchers now believe that Thymosin beta-4 changes cell metabolism to create stronger heart muscle cells that can resist the low oxygen conditions after a heart attack.

The next step, Srivastava said, is to determine the most effective dose, the optimal time to administer Thymosin beta-4 and how long after an attack the protein can be given to be effective.

EARLIER RESEARCH

Last year Srivastava and his team identified a gene that plays a role in the development of heart defects, especially in children.

The gene, known as GATA4, is only the second gene that´s been identified as a possible cause of congenital heart defects, one of the most common birth defects in the United States.

"This gene is in a class of master regulators. It turns other genes on or off," said Srivastava. A mutation in this gene affects its function, says Srivastava, which prevents GATA4 from turning on other genes that are responsible for tasks such as forming a baby´s heart walls early in pregnancy.

The result is a congenital heart defect, often literally a hole in the heart or a problem with the heart´s valves. Slightly less than 1 percent of American babies, or about 35,000 annually, have a congenital heart defect, according to the American Heart Association. Congenital heart defects remain the leading birth defect-related cause of death in infants, according to the March of Dimes.

Knowing the cause may eventually lead to therapies for prevention in much the same way that folic acid has helped reduce neural tube defects, another class of birth defects, says Srivastava.

"The most immediate application is for families that have the mutation," he says. "We can provide very accurate genetic counseling and can test for the mutation. If the parents have the mutation, the risk of passing it on is 50 percent. If they don´t have the mutation, the risk is zero percent."

Srivastava predicts: “We are beginning an exciting and revolutionary era in biology and medicine that should transform our approach to treatment and prevention of human disease. It is tempting to declare that the future is now, but many challenges lie ahead.”

Ongoing studies are building the foundation for future preventive and therapeutic interventions for congenital heart defects which involve about 25,000 babies born in the United States each year, or as many as one in 125 births, according to the March of Dimes. Many defects require open-heart surgery to repair.

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