High blood pressure also called hypertension is the leading cause of death globally affecting more than 1 billion people. Hypertension is the major risk factor for stroke, heart failure and kidney disease.
A new study published in the journal Immunity revealed that a protein in the spleen, placental growth factor (PGIF) plays a critical role in activating a harmful immune response leading to high blood pressure.
The theory was tested in mice models and mounting evidence suggests that immune cells such as T cellscontribute to the development of hypertension. PGIF appears to be the critical factor involved as it plays an important role in both the cardiovascular system and the immune system.
Mice that were genetically engineered to lack PlGF did not develop hypertension after they were infused with angiotensin II–a hormone that normally increases blood pressure. These mice were also protected from hypertension-related heart and kidney damage, unlike genetically normal mice. Moreover, PlGF deficiency prevented T cells from leaving the spleen, entering the blood stream, and infiltrating the vessels and kidneys where hypertension was manifested. Additional experiments revealed that the nervous system controls levels of PlGF in the spleen, and PlGF in the spleen in turn is essential for the activation of T cells and the onset of hypertension.
“In recent years, anti-PlGF monoclonal antibodies have been developed as a strategy to slow tumor growth and for age-related macular degeneration,” says lead study author Daniela Carnevale. “The ongoing clinical trials testing humanized monoclonal antibodies directed to PlGF opens up the possibility of targeting it in hypertension too.”
“There is a pressing need for new treatments to control and better target resistant hypertension,” says Lembo. “PlGF is an appealing molecular therapeutic target because clinical tools to target this pathway already exist.”
The angiogenic factor PlGF mediates a neuroimmune interaction in the spleen to allow the onset of hypertension. Carnevale et al. Immunity, 2014. DOI:S1074-7613(14)00397-5