Murine atherosclerosis models do not spontaneously develop atherothrombotic complications. We investigated whether disruption of natural anticoagulation allows preexisting atherosclerotic plaques... Show moreMurine atherosclerosis models do not spontaneously develop atherothrombotic complications. We investigated whether disruption of natural anticoagulation allows preexisting atherosclerotic plaques to progress toward an atherothrombotic phenotype. Mice featured clots in the left atrium of the heart. Our findings indicate that small interfering RNA-mediated silencing of protein C in apolipoprotein E-deficient mice creates a condition that allows the occurrence of spontaneous atherothrombosis, albeit at a low incidence. Lowering natural anticoagulation in atherosclerosis models may help to discover factors that increase atherothrombotic complications. Show less
Ouweneel, A.B.; Heestermans, M.; Verwilligen, R.A.F.; Eck, M. van; Vlijmen, B.J.M. van 2016
Objectives: Studies on atherothrombosis, a major cause of cardiovascularevents, are hampered by the lack of animal models spontaneously developingatherothrombosis. Major underlying problems are the... Show moreObjectives: Studies on atherothrombosis, a major cause of cardiovascularevents, are hampered by the lack of animal models spontaneously developingatherothrombosis. Major underlying problems are the stability ofthe atherosclerotic plaques, combined with the strong plasma anticoagulantactivity. We hypothesized that inhibition of the anticoagulant systemby silencing of protein C (Proc) may cause murine atherosclerotic plaquesto become prone to atherothrombosis. Show less
