Critical role of bone marrow angiotensin II type 1 receptor in the pathogenesis of atherosclerosis in apolipoprotein E-deficient mice
Critical role of bone marrow angiotensin II type 1 receptor in the pathogenesis of atherosclerosis in apolipoprotein E-deficient mice
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DOI：
10.1161/atvbaha.107.152363
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发表时间：
2008-01-01
影响因子：
8.7
通讯作者：
Nagai, Ryozo
中科院分区：
文献类型：
--
作者：
Fukuda, Daiju;Sata, Masataka;Nagai, Ryozo
目的：血管紧张素II(Ang II)-血管紧张素II 1型受体(AT1R)通路在动脉粥样硬化的发病机制中起重要作用。最近，有报道骨髓细胞表达AT1R。在这里，我们研究了AT1R在BM中在动脉粥样硬化发病机制中的作用。方法和结果-AT1R的遗传消融或药物阻断导致ApoE(-/-)小鼠动脉粥样硬化病变显著减少和稳定。为了阐明AT1R在BM中的作用，我们产生了几只BM嵌合小鼠。无论受体血管系统中是否存在AT1aR，Ang II均可促进BM中AT1aR表达的嵌合小鼠的动脉粥样硬化进展(P
Objective-It is suggested that the angiotensin II (Ang II)-Ang II type 1 receptor (AT1R) pathway plays a pivotal role in the pathogenesis of atherosclerosis. Recently, bone marrow (BM) cells were reported to express AT1R. Here, we investigated the role of AT1R in BM in the pathogenesis of atherosclerosis.Methods and Results-Genetic ablation or pharmacological blockade of AT1R led to a significant reduction and stabilization of atherosclerotic lesions in ApoE(-/-) mice. To elucidate the role of AT1R in BM, we generated several BM chimeric mice. Ang II promoted atherosclerosis progression in the BM chimeric mice that had AT1aR in BM, regardless of the absence of AT1aR in the recipient vasculature (P