Angiotensin II induces extracellular matrix metalloproteinase inducer expression via an AT1R dependent pathway in aortic atherosclerotic plaque in apolipoprotein E knockout mice
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چکیده
منابع مشابه
A selective matrix metalloproteinase-12 inhibitor retards atherosclerotic plaque development in apolipoprotein E-knockout mice.
OBJECTIVE Matrix metalloproteinase (MMP)-12 has been implicated in plaque progression and instability and is also amenable to selective inhibition. In this study, we investigated the influence of a greater than 10-fold selective synthetic MMP-12 inhibitor on plaque progression in the apolipoprotein E knockout mouse model of atherosclerosis. METHODS AND RESULTS A phosphinic peptide (RXP470.1) ...
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A therosclerotic plaque rupture and subsequent thrombus formation in the culprit lesion are recognized to be the seminal events in the majority of cases of acute coronary syndrome. Plaque stability is determined by many factors, including lipid deposits, oxidative stress, inflammation, and extracellular matrix degradation. Accumulation of lipid in the atherosclerotic lesion increases mechanical...
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UCP-2 shows an important role in modulating of mitochondrial membrane potential and cell apoptosis. Whether or not UCP-2 could been a critical factor in preventing AAA formation is not known. We report that UCP-2 protein and mRNA expression were significantly higher in Ang-Ⅱ-induced AAA of mice. The incident rate of AAA in UCP-2-/-ApoE-/- mice after Ang-Ⅱtreatment was higher than the rate in th...
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Atherosclerotic plaque rupture and local thrombosis activation in the artery cause acute serious incidents such as acute coronary syndrome and stroke. The exact mechanism of plaque rupture remains unclear but excessive degradation of the extracellular matrix scaffold by matrix-degrading metalloproteinases (MMPs) has been implicated as one of the major molecular mechanisms in this process. Convi...
متن کاملAngiotensin II-induced TLR4 mediated abdominal aortic aneurysm in apolipoprotein E knockout mice is dependent on STAT3.
Abdominal Aortic Aneurysm (AAA) is a major cause of mortality and morbidity in men over 65 years of age. Male apolipoprotein E knockout (ApoE(-/-)) mice infused with angiotensin II (AngII) develop AAA. Although AngII stimulates both JAK/STAT and Toll-like receptor 4 (TLR4) signaling pathways, their involvement in AngII mediated AAA formation is unclear. Here we used the small molecule STAT3 inh...
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ژورنال
عنوان ژورنال: Journal of the Renin-Angiotensin-Aldosterone System
سال: 2011
ISSN: 1470-3203,1752-8976
DOI: 10.1177/1470320311423780