Resolving arterial calcification
A serious complication of inflammatory disease is arterial calcification, a condition caused by calcium deposition along arterial walls. This severely disrupts the regenerative capacity of specific cells, culminating in vessel constriction, compromised wall elasticity and reduced blood flow. In turn, this can lead to cardiovascular disease, end stage renal disease or peripheral arterial disease. The primary objective of the EU-funded ACAR (Arterial Calcification & Arterial Regeneration ‘ACAR’) project was to identify calcification biomarkers in vascular smooth muscle cells and investigate the regenerative potential of endothelial progenitor cells (EPCs). From a therapeutic perspective, researchers are interested to test the influence of vitamin K and selenium on calcification processes and examine biomarker expression on these EPCs. ACAR established a cell culture facility in the host laboratory during the first project period. They also equipped it with all the necessary cell lines and reagents. For instance, they set up EPC culture assays from peripheral arterial disease patients and controls. Considerable effort has also gone into finalising the working protocols and standard operating procedures. Experiments in animal models have uncovered biomarkers involved in calcification but very little is known in humans. ACAR researchers plan to investigate two calcification mechanisms, namely warfarin and oxidative stress. Warfarin is an anticoagulant and inducer of calcification in certain cells, while oxidative stress is known to affect various cellular mechanisms including calcification. Collectively the ACAR study should help unveil the mechanisms of arterial calcification and identify related biomarkers in human cells. Importantly it should offer putative interventions that could also apply to other inflammatory diseases.
Keywords
Arterial calcification, inflammatory disease, endothelial progenitor cells, warfarin, oxidative stress
