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Neighbor Fight Off Home Invasion SuspectsDeterioration of atherosclerosis in mice lacking angiotensin II type 1A receptor in bone marrow derived cellsHideki Kato1,2, Junji Ishida1, Katsumasa Nagano1, Kaori Honjo1, Takeshi Sugaya1, Norifumi Takeda3, Fumihiro Sugiyama4, Ken ichi Yagami4, Toshiro Fujita2, Masaomi Nangaku2 and Akiyoshi Fukamizu1Received 26 September 2007; Revised 3 March 2008; Accepted 7 March 2008; Published online 19 May 2008. Top of pageAbstractThe renin system (RAS) modulates end Nike Roshe Run Knit Jacquard

There was no difference in the extent of kidney damage between mice receiving BM transplants from mutant mice lacking the angiotensin II type 1a receptor (AT1a) gene and mice receiving transplants from wild type (WT) mice. However, mice receiving transplants from AT1a (KO) mice displayed accelerated lethality and atherosclerotic lesions. These results indicated that the effects of AT1a receptor on BMDCs are organ dependent.

Nike Roshe Run Grey

Nike Roshe Run Grey

Nike Roshe Run Grey

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Nike Roshe Run Grey

Nike Roshe Run Grey

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organ damages, resulting in cardiovascular and kidney diseases. Experiments both in vitro and in vivo demonstrate that the angiotensin II (Ang II) type 1 (AT1) receptor pathway also exerts pro inflammatory and pro atherogenic effects on bone marrow derived cells (BMDCs). Here, we investigated how AT1 receptor expression by BMDCs contributes to atherosclerosis and kidney injury in vivo by transplanting BM into RAS activated transgenic mice.

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Microarray expression profiling of macrophages from AT1a KO mice revealed significant changes in the mRNA levels for a number of genes implicated in atherosclerosis. In accordance with the in vivo atherosclerosis results, AT1.

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