A survival strategy for the cells lining our blood vessels

The role of nitric oxide / cyclic GMP / β-catenin signalling in endothelial cell survival in the vasculature

Professor Albert Ferro and his colleagues at King’s College London are studying how a process called apoptosis, or programmed cell death, is involved in heart and circulatory disease. Endothelial cells line the inner surface of all blood vessels and are constantly renewing themselves - old cells die and new cells replace them. This is part of the body’s natural repair system. But in heart and circulatory diseases, including atherosclerosis (the process underlying coronary heart disease) and heart failure, too many endothelial cells undergo programmed cell death. Boosting cell survival may help to prevent or treat these conditions. We already know that two signalling molecules, nitric oxide (NO) and beta-catenin can boost cell survival. Professor Ferro has discovered that NO produced by endothelial cells also activates beta-catenin, which itself can increase NO production. This suggests that cross-talk between NO and beta-catenin may encourage endothelial cell to survive by blocking apoptosis. In this project, Professor Ferro will work out how NO and beta-catenin promote endothelial cell survival. He will find out whether the drug sildenafil, which increases NO signalling, blocks apoptosis and encourages endothelial cells to survive. This research will give us a better understanding of the mechanisms controlling endothelial cell survival and death. It may reveal a new drug that could ultimately help to prevent or treat heart and circulatory disease in the future.