Nitric oxide regulates Angiopoietin1/Tie2 expression after stroke

被引:32
作者
Zacharek, Alex
Chen, Jieli
Zhang, Chunling
Cui, Xu
Roberts, Cynthia
Jiang, Hao
Teng, Hua
Chopp, Michael
机构
[1] Henry Ford Hlth Sci Ctr, Dept Neurol, Detroit, MI 48202 USA
[2] Oakland Univ, Dept Phys, Rochester, MI 48309 USA
关键词
angiogenesis; DETA-NONOate; Angiopoietin; 1; Tie2; Occludin; stroke;
D O I
10.1016/j.neulet.2006.05.027
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We tested whether the nitric oxide donor, (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) aminio] diazen-1-ium-1,2-diolate (DETA-NONOate), increases expression of Angiopoietin (Ang1)/Fie2, which may playa role in regulating angliogenesis and vascular integrity after stroke in rats. Wistar rats were subjected to middle cerebral artery occlusion and treated with or without DETA-NONOate. Stroke rats treated with DETA-NONOate show significantly increased Ang1, Tic2 and Occludin expression in the ischemic border compared with control stroke animals (P < 0.05). Consistent with in vivo data, DETA-NONOate promotes capillary tube formation in cultured brain endothelial cells. Neutralizing Angl antibody attenuates DETA-NONOate-induced capillary tube formation. The data suggest that the Ang1/Tie2 axis promotes DETA-NONOate-induced angiogenesis and stabilizes of angiogenic vessels after stroke. (c) 2006 Published by Elsevier Ireland Ltd.
引用
收藏
页码:28 / 32
页数:5
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