Reduced calcification and osteogenic features in advanced atherosclerotic plaques of mice with macrophage-specific loss of TRPC3.
Reduced calcification and osteogenic features in advanced atherosclerotic plaques of mice with macrophage-specific loss of TRPC3.
复制标题
DOI：
10.1016/j.atherosclerosis.2017.12.025
复制
发表时间：
2018-03
期刊：
影响因子：
5.3
通讯作者：
Vazquez G
中科院分区：
文献类型：
--
作者：
Dube PR;Chikkamenahalli LL;Birnbaumer L;Vazquez G
Recent in vitro studies have showed that in macrophages deletion of the non-selective Ca2+-permeable channel TRPC3 impairs expression of the osteogenic protein BMP-2. The pathophysiological relevance of this effect in atherosclerotic plaque calcification remains to be determined. We used Ldlr−/− mice with macrophage-specific loss of TRPC3 (MacTrpc3−/−/Ldlr−/−) to examine the effect of macrophage Trpc3 on plaque calcification and osteogenic features in advanced atherosclerosis. After 25 weeks on high fat diet, aortic root plaques in MacTrpc3−/−/Ldlr−/− mice showed reduced size, lipid and macrophage content compared to controls. Plaque calcification was decreased in MacTrpc3−/−/Ldlr−/− mice, and this was accompanied by marked reduction in BMP-2, Runx-2 and phospho-SMAD1/5 contents within macrophage-rich areas. Expression of Bmp-2 and Runx-2 was also reduced in bone marrow-derived macrophages from MacTrpc3−/−/Ldlr−/− mice. These findings show that, in advanced atherosclerosis, selective deletion of TRPC3 in macrophages favors plaque regression and impairs the activity of a novel macrophage-associated, BMP-2-dependent mechanism of calcification.
登录
查看更多内容
影响因子：
4.6
作者：
Solanki S;Dube PR;Birnbaumer L;Vazquez G
通讯作者：
Vazquez G
DOI：
10.1007/978-3-319-05161-1_14
发表时间：
2014-01-01
期刊：
MAMMALIAN TRANSIENT RECEPTOR POTENTIAL (TRP) CATION CHANNELS, VOL II
影响因子：
--
作者：
Liao, Yanhong;Abramowitz, Joel;Birnbaumer, Lutz
通讯作者：
Birnbaumer, Lutz
DOI：
10.1161/01.atv.0000166600.58468.1b
发表时间：
2005-07-01
影响因子：
8.7
作者：
Rattazzi, M;Bennett, BJ;Rosenfeld, ME
通讯作者：
Rosenfeld, ME
影响因子：
20.1
作者：
Smedlund, Kathryn;Tano, Jean-Yves;Vazquez, Guillermo
通讯作者：
Vazquez, Guillermo
影响因子：
30.5
作者：
通讯作者：
--