The observations were presented at the American Heart Association's Basic Cardiovascular Sciences 2010 Scientific Sessions

Jul 21, 2010 08:03 GMT  ·  By

A new study on rats, presented at the American Heart Association's Basic Cardiovascular Sciences 2010 Scientific Sessions – Technological and Conceptual Advances in Cardiovascular Disease, concluded that platforms with genetically engineered stem cells helped reduce organ damage after a heart attack. A cardiac function improvement was also noticed.

The study was lead by Matthias Siepe, M.D., assistant professor and staff surgeon at the Department of Cardiovascular Surgery, Medical University Center in Freiburg, Germany, and its goal was to see the effect of cytokines after a heart attack. Cytokines are substances secreted by cells with an impact on other cells.

Five groups of 10 rats each were implanted small polyurethane platforms with different genetically modified stem cells. Cells that overproduced one of three cytokines: hepatocyte growth-factor (HGF), vascular endothelial growth factor (VEGF) or stromal cell-derived factor 1 (SDF-1), were administrated to three of the groups; a gene associated with several cytokine pathways, called Akt1 was given to the fourth group and the last one, received unmodified stem cells. Another five groups were given the same types of stem cells, but without the scaffolding. Also, an 11th control group received a fake operation, Siepe said. This procedure is similar to the others except it lacks a key therapeutic compound of the treatment.

The rats were followed for six weeks and at the end, scientists noticed significant blood pressure improvements in rats that were given scaffolds with stem cells that overproduced SDF-1, HGF and Akt1. The group having received scaffolds with vascular endothelial growth factor showed no functional change.

On the other side, the group that received the fake procedures had a decrease in blood pressure functioning, and it remained stable for rats having received scaffolds of unmodified stem cells. Also, SDF-1 and Akt1 overproduction presented a limitation of cardiac damage triggered by the heart attack.