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Scarring a necessary evil to prevent further damage after heart attack
Date:11/15/2011

like in zebrafish where the epicardium contributed to generation of heart muscle cells, in the mouse the epicardium generated fibroblasts, the fibrous cells that underlie scar tissue.

The researchers then found that a protein called Wnt1, which they had formerly shown to enhance function of human vascular stem cells, was driving stem cells within the epicardium to become fibroblasts. They wondered if interrupting this molecular pathway could ameliorate scarring and improve heart function. Surprisingly, when they interrupted Wnt1 signaling in genetically engineered mice, the mutants developed heart failure within 2 weeks after cardiac injury.

"There are clearly evolutionary parallels between the zebrafish and the mouse, but there must be some sort of a selection pressure in mammals to respond to heart injury by scarring, because if we interrupt this process then the heart quickly fails following injury," said Deb. "In organisms where there is a high pressure of blood flow, these cells may need to turn into scar tissue to maintain the tensile strength of the heart wall and prevent catastrophic rupture," speculates Deb.

Now Deb and his colleagues are genetically manipulating the stem cells residing in the epicardium at later time points to see if they can coax them to stop turning into fibroblasts and start forming heart-regenerating myocytes. If so, the approach could prove to be an invaluable way to help patients recover from a heart attack.


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Contact: Les Lang
llang@med.unc.edu
919-966-9366
University of North Carolina School of Medicine
Source:Eurekalert  

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