Intensive research work
In 1984, the newly elected director of the Wihuri Research Institute, Docent Vesa Manninen, asked for my assistance in a research project initiated by Professor Pentti Halonen before his retirement. The project had an interesting non-mainstream research question that was typical of Prof. Halonen: how histamine release from mast cells might affect the blood lipid metabolism of a rabbit that had been fed cholesterol. That was the beginning of intensive research work with my colleague Jorma Kokkonen, research that I have continued to do until this day with different teams. I quickly altered the original research strategy: I was not interested in LDL cholesterol metabolism in the blood, but rather at the cellular level in the arterial wall. Thus began the still ongoing series of research projects to determine the effects of mast cells in the arterial wall on the pathogenesis of atherosclerosis. What happens to LDL and HDL lipoprotein particles in the arterial wall in the early stage of the disease, and how can mast cells affect the structure of the atherosclerotic plaque formed on the arterial wall in the late stage? I had the opportunity to discuss these research results with leading international researchers in 1989 during the symposium “Lipoproteins and Pathobiology of the Arterial Intima” supported by the Paavo Nurmi Foundation and held at Haikko Manor, Finland.
We have observed mast cells in the walls of atherosclerotic arteries. The more advanced the stage of the disease, the more mast cells there are in the arteries. The mast cells in atherosclerotic plaque are activated to secrete proteases, enzymes that break down proteins, into their environment. These enzymes may accelerate the accumulation of cholesterol in the plaque, and may subsequently weaken the structure of the plaques, making them more likely to rupture and cause atherothrombotic complications. Thus, mast cells in an atherosclerotic coronary artery may play a part in the pathogenesis of myocardial infarction, while the mast cells in an atherosclerotic carotid artery may make a person vulnerable to cerebrovascular disorders and trigger a stroke. Mast cells in a distended atherosclerotic aorta may weaken the structure of the aorta and increase the risk of aortic rupture