منابع مشابه
Mouse model of arterial injury.
In the present study, we established an injury model of the mouse carotid artery. Complete removal of the endothelium was achieved with a flexible wire. A platelet monolayer covered the denuded surface, and damage to underlying medial smooth muscle cells (SMCs) was detected. Injection of [3H]thymidine was used to determine the replication index for medial SMCs, which was found to be 1.6% at 2 d...
متن کاملThe effect of tyrphostin AG-556 on intimal thickening in a mouse model of arterial injury.
BACKGROUND Inflammation has been shown to play an important role in promoting the response to arterial injury and proinflammatory cytokines, such as tumor necrosis factor (TNF) alpha, are candidate mediators. AG-556 is a tyrosine kinase inhibitor proven to be effective in a model of multiple sclerosis-like syndrome in mice due to its immunomodulating effect. In the current study, we investigate...
متن کاملDecreased reendothelialization and increased neointima formation with endostatin overexpression in a mouse model of arterial injury.
BACKGROUND Impaired endothelial regeneration contributes to arterial lesion formation. Endostatin is a specific inhibitor of endothelial cell growth and induces endothelial cell apoptosis. We examined the effect of endostatin overexpression on reendothelialization and neointima formation in a mouse model of arterial injury. METHODS AND RESULTS Mice underwent femoral arterial denudation and re...
متن کاملVascular endothelial growth factor regulates reendothelialization and neointima formation in a mouse model of arterial injury.
BACKGROUND The rate of reendothelialization is critical in neointima formation after arterial injury. Vascular endothelial growth factor (VEGF), a potent endothelial mitogen, has been advocated for accelerating endothelial repair and preventing intimal hyperplasia after percutaneous coronary interventions. However, the precise mechanism of action of VEGF treatment and the physiologic role of en...
متن کاملRosiglitazone reduces the accelerated neointima formation after arterial injury in a mouse injury model of type 2 diabetes.
BACKGROUND Hyperglycemia (HG) and hyperinsulinemia (HI) may be factors enhancing the atherosclerotic complications of diabetes. We hypothesized that specific feeding of C57BL/6 apolipoprotein (apo) E-/- mice would alter their metabolic profiles and result in different degrees of neointima (NI) formation. We additionally hypothesized that an insulin-sensitizing agent (rosiglitazone) would preven...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 1993
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.73.5.792