Scientists identify molecule that prompts damaged heart to repair itself

April 11th, 2009 - 2:48 pm ICT by ANI  

Washington, Apr 11 (ANI): Researchers from UT Southwestern Medical Centre have identified a molecule that prompts damaged heart cells to repair themselves after a heart attack.

The research team led by Drs. J. Michael DiMaio and Ildiko Bock-Marquette has discovered a molecule called, Thymosin beta-4 (TB4), which is expressed by embryos during the heart’s development and encourages migration of heart cells.

They showed that introducing TB4 systemically after a heart attack encourages new growth and repair of heart cells as early as 24 hours after systemic injection.

In the mouse study, researchers found that TB4 initiates capillary tube formation of adult coronary endothelial cells in tissue culture.

It also encourages cardiac regeneration by inhibiting death in heart cells after an injury such as a heart attack and by stimulating new vessel growth.

“This molecule has the potential to reprogram cells in the body to get them to do what you want them to do,” said Dr. DiMaio, associate professor of cardiothoracic surgery at UT Southwestern and senior author of the study.

“Obviously, the clinical implications of this are enormous because of the potential to reverse damage inflicted on heart cells after a heart attack,” he added.

“We observed that by injecting this protein systemically, there was increased cardiac function after a heart attack,” said Dr Bock-Marquette, assistant professor of cardiothoracic surgery at UT Southwestern and the study’s lead author.

“We hope this protein can inhibit cell death that occurs during a heart attack in the short term, and that it may initiate new growth of coronary vessels by activating progenitor cells in the long term,” Bock-Marquette added.

The researchers will be conducting further studies to examine whether the same events occur in larger mammals and which receptors are responsible for the action of this molecule.

The study appears in Journal of Molecular and Cellular Cardiology. (ANI)

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