C1-Esterase Inhibitor Protects Against Neointima Formation After Arterial Injury in Atherosclerosis-Prone Mice
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چکیده
منابع مشابه
C1-esterase inhibitor protects against neointima formation after arterial injury in atherosclerosis-prone mice.
BACKGROUND Although activation of the complement system has been implicated in the progression of human atherosclerosis, its function during arterial remodeling after injury has not been investigated. Here, we examined the contribution of the complement cascade to neointima formation in apolipoprotein E-deficient mice using a C1-esterase inhibitor (C1-inhibitor). METHODS AND RESULTS Apolipopr...
متن کاملVascular Medicine C5a Receptor Targeting in Neointima Formation After Arterial Injury in Atherosclerosis-Prone Mice
Background—Receptor binding of complement C5a leads to proinflammatory activation of many cell types, but the role of receptor-mediated action during arterial remodeling after injury has not been studied. In the present study, we examined the contribution of the C5a receptor (C5aR) to neointima formation in apolipoprotein E–deficient mice employing a C5aR antagonist (C5aRA) and a C5aR-blocking ...
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BACKGROUND Receptor binding of complement C5a leads to proinflammatory activation of many cell types, but the role of receptor-mediated action during arterial remodeling after injury has not been studied. In the present study, we examined the contribution of the C5a receptor (C5aR) to neointima formation in apolipoprotein E-deficient mice employing a C5aR antagonist (C5aRA) and a C5aR-blocking ...
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The hypothesis that tissue inhibitor of metalloproteinases-1 (TIMP-1) plays a role in neointima formation was tested with the use of a vascular injury model in wild-type (TIMP-1(+/+)) and TIMP-1-deficient (TIMP-1(-/-)) mice. The neointimal area at 1 to 3 weeks after electric injury of the femoral artery was significantly higher in TIMP-1(-/-) as compared with TIMP-1(+/+) mice (0.012+/-0. 0015 v...
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ژورنال
عنوان ژورنال: Circulation
سال: 2008
ISSN: 0009-7322,1524-4539
DOI: 10.1161/circulationaha.107.715649