Regulation of the switch to pathogenic angiopoietin signalling and its involvement in cardiovascular diseases
People who have had heart attacks, heart failure or need a heart transplant have high levels of a protein called Ang2 in their blood. In these people, there is a switch in their blood vessels that makes them respond differently to Ang2. This switch causes blood vessel damage and leads to injury of the heart, lungs and other organs. In blood vessel cells, Ang2 works with another molecule called Tie2, which is bound together with Tie1. The loss of Tie1 switches the effects of Ang2 from protective to harmful, but exactly how this loss of Tie1 occurs is not known. Professor Brindle’s team at the University of Leicester have previously found that molecules called integrins have crucial roles in ensuring Tie1 remains in blood vessel cells. This project will now build on this discovery to determine how integrins regulate the release of Tie1. They will also investigate the relationship between Tie1 loss in blood vessel cells with heart and circulatory diseases, by examining human blood samples. This study should provide a new understanding of the fundamental mechanism regulating the switch from protective to harmful communication in blood vessels. This may help the development of new treatments for heart and circulatory diseases in the future.
Project details
| Grant amount | £158,770 |
|---|---|
| Grant type | Project Grants |
| Application type | Project Grant |
| Start Date | 02 September 2019 |
| Duration | 2 years |
| Reference | PG/19/27/34305 |
| Status | In Progress |
