Silencing of Anticoagulant Protein C Evokes Low-Incident but Spontaneous Atherothrombosis in Apolipoprotein E-Deficient Mice-Brief Report

Ouweneel, A.B.; Heestermans, M.; Verwilligen, R.A.F.; Gijbels, M.J.J.; Reitsma, P.H.; Eck, M. van; Vlijmen, B.J.M. van (2017)

Article / Letter to editor

Murine 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.

• Anticoagulation
• Atherosclerosis
• Atherothrombosis
• Mouse models
• Protein C

• All authors: Ouweneel, A.B.; Heestermans, M.; Verwilligen, R.A.F.; Gijbels, M.J.J.; Reitsma, P.H.; Eck, M. van; Vlijmen, B.J.M. van
• Date: 2017-03-01
• Volume: 37
• Issue: 5
• Pages: 782 - 785
• DOI: doi:10.1161/ATVBAHA.117.309188