How does cAMP exert anti-inflammatory effects in blood vessels?

The role of nuclear actin dynamics in the regulation of vascular smooth muscle cell inflammation (Mr Joeseph Hawkins)

Bristol researchers are testing their theory of how blood vessel-damaging inflammation occurs in the body. Inflammation is an essential process for healthy healing after injury. However, long-term inflammation is involved in many heart and circulatory problems, including coronary heart disease, aneurysm and heart bypass failure. We have yet to discover ways to reduce inflammation in ways that help protect against problems in our circulatory system. More research is needed to understand how much inflammation is too much. Previous research has shown that when levels of a molecule called cAMP are raised in the body, there is an anti-inflammatory effect. We don’t yet understand how and why cAMP exerts these potentially beneficial effects. Dr Bond’s group have found that cAMP can increase levels of a protein called actin inside the nucleus of blood vessel cells. This is interesting because actin is a ‘structural’ protein that normally acts outside of the nucleus. Their preliminary data indicates that cAMP causes actin to enter the nucleus, where it is able to block molecules that switch on certain pro-inflammatory genes. In this project they will now test their theory and build on their preliminary data. This could provide new ways to limit the inflammation that underlies many heart and circulatory diseases.