Level of macrophage uPA expression is an important determinant of atherosclerotic lesion growth in Apoe-/- mice.

Objective: Enhanced plasminogen activation, mediated by overexpression of urokinase-type plasminogen activator (uPA), accelerates atherosclerosis in apolipoprotein E-null mice. However, the mechanisms through which uPA acts remain unclear. In addition, although elevated uPA expression can accelerate murine atherosclerosis, there is not yet any evidence that decreased uPA expression would retard atherosclerosis.

Incidence of atypical handedness in epilepsy and its association with clinical factors.

The incidence of atypical handedness (left-handedness and ambidexterity) in patients with epilepsy, particularly its association with major clinical factors, is not well established. We evaluated a full range of clinical variables in 478 patients with epilepsy from the United States and Korea. With the Edinburgh Handedness Inventory, handedness was established as both a categorical variable (right-handed, left-handed, ambidextrous) and a continuous variable.

Plasminogen mediates the atherogenic effects of macrophage-expressed urokinase and accelerates atherosclerosis in apoE-knockout mice.

Urokinase-type plasminogen activator (uPA) is expressed at elevated levels in atherosclerotic human arteries, primarily in macrophages. Plasminogen (Plg), the primary physiologic substrate of uPA, is present at significant levels in blood and interstitial fluid. Both uPA and Plg have activities that could affect atherosclerosis progression.

Macrophage-targeted overexpression of urokinase causes accelerated atherosclerosis, coronary artery occlusions, and premature death.

Background: Human atherosclerotic lesions contain elevated levels of urokinase plasminogen activator (uPA), expressed predominantly by macrophages.

Methods And Results: To test the hypothesis that macrophage-expressed uPA contributes to the progression and complications of atherosclerosis, we generated transgenic mice with macrophage-targeted overexpression of uPA. The uPA transgene was bred into the apolipoprotein E-null background, and transgenic mice and nontransgenic littermate controls were fed an atherogenic diet.