Urokinase-Type Plasminogen Activator Plays a Critical Role in Angiotensin II-induced Abdominal Aortic Aneurysm

Abstract

In a previous study in apolipoprotein E-deficient mice treated with angiotensin II (Ang II), the authors demonstrated that urokinasetype plasminogen activator (uPA) is highly expressed in the aneurysmal segment of the abdominal aorta. The authors conducted the present study to determine if uPA is essential for the formation of abdominal aortic aneurysm (AAA) in this same mouse model. Male mice were implanted for 1 month with a subcutaneous osmotic minipump that delivered 1.44 mg/kg per day of Ang II. AAA was induced in 90% of apoE deficient mice, but only 22% of the mice deficient in both apoE and uPA developed AAA. In 18 strainmatched wild type control mice, Ang 11 induced AAA in 39%. The author's concluded that a uPA deficiency has a protective effect against Ang II-induced AAA development, that uPA is not required for normal vascular development and maintenance, and that preexisting hyperlipidemia and atherosclerosis are not essential for Ang II-induced AAA formation.