A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization.
A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization.
复制标题
DOI：
10.1016/j.atherosclerosis.2010.03.029
复制
发表时间：
2010-08
期刊：
影响因子：
5.3
通讯作者：
Ferran, Christiane
中科院分区：
文献类型：
--
作者：
Damrauer, Scott M.;Fisher, Mark D.;Wada, Hiromi;Siracuse, Jeffrey J.;da Silva, Cleide G.;Moon, Karam;Csizmadia, Eva;Maccariello, Elizabeth R.;Patel, Virendra I.;Studer, Peter;Essayagh, Sanah;Aird, William C.;Daniel, Soizic;Ferran, Christiane
Neointimal hyperplasia is an inflammatory and proliferative process that occurs as a result of injury to the vessel wall. We have shown that the homeostatic protein A20 prevents neointimal hyperplasia by affecting endothelial cell (EC) and smooth muscle cell (SMC) responses to injury. In this work, we questioned whether A20 impacts other pathogenic effectors of neointimal hyperplasia including homing of monocyte/macrophages and EC/SMC precursors to the site of vascular injury, vascular endothelial growth factor (VEGF) secretion, and adventitial neovascularization. Carotid balloon angioplasty was performed on rat recipients of a bone marrow transplant from green fluorescent rats. Adenoviral delivery of A20 prevented neointimal hyperplasia and decreased macrophage infiltration. This was associated with decreased ICAM-1 and MCP-1 expression in vitro. Additionally, A20 reduced neovascularization in the adventitia of balloon injured carotid arteries, which correlated with fewer VEGF positive cells. A20 down-regulates adhesion markers, chemokine production, and adventitial angiogenesis, all of which are required for macrophage trafficking to sites of vascular injury. This, in turn, diminishes the inflammatory milieu to prevent neointimal hyperplasia.
登录
查看更多内容
影响因子：
5.3
作者：
Squadrito, F;Deodato, B;Altavilla, D
通讯作者：
Altavilla, D
影响因子：
11
作者：
Wang, Ai-Bing;Li, Hong-Liang;Liang, Chih-Chuan
通讯作者：
Liang, Chih-Chuan
影响因子：
5.2
作者：
Westerband, A;Gentile, AT;Mills, JL
通讯作者：
Mills, JL
影响因子：
37.8
作者：
Ohtani, K;Egashira, K;Sunagawa, K
通讯作者：
Sunagawa, K
影响因子：
4.8
作者：
Kim, I;Moon, SO;Koh, GY
通讯作者：
Koh, GY