The study published in "Cell Reports" originated with scientists led by Christoph Binder, Group Leader at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and atherosclerosis researchers at the Medical University of Vienna.
In occurrences of vascular calcification, “bad” LDL cholesterol is stored in vascular walls. Harmful oxygen radicals arise on the basis of oxidation, which in turn cause the inflammation. Macrophages (scavenger cells) move to the walls of the arteries and bind the oxidized LDL blood fat, convert them into foam cells and further strengthen the inflammation through immune system messengers.
A certain group of white blood cells – B-1 cells – work against the life-threatening damage to vessels that can lead to heart attack and stroke. These cells produce naturally occurring antibodies that bind oxidized LDL and neutralize it, disrupting the inflammation. The immune cells also carry a molecular regulator that reduces their activity, said Sabrina Gruber, the first author of the study and PhD student at CeMM.
“We were able to show that the deactivation of this regulator, the so-called 'Siglec-G' protein, caused an increased propagation of B1-cells and antibodies, which protect vessels and the liver from inflammation”, the scientist added.