ECTOPIC EXPRESSION OF HUMAN ANGIOPOIETIN-1 PROMOTES FUNCTIONAL RECOVERY AND NEUROGENESIS AFTER FOCAL CEREBRAL ISCHEMIA
ECTOPIC EXPRESSION OF HUMAN ANGIOPOIETIN-1 PROMOTES FUNCTIONAL RECOVERY AND NEUROGENESIS AFTER FOCAL CEREBRAL ISCHEMIA
复制标题
人血管生成素-1的异位表达促进局灶性脑缺血后的功能恢复和神经发生
DOI：
10.1016/j.neuroscience.2014.02.036
复制
发表时间：
2014-05-16
期刊：
影响因子：
3.3
通讯作者：
Bai, Y.
中科院分区：
文献类型：
--
作者：
Meng, Z.;Li, M.;Bai, Y.
神经病理过程如脑缺血可增强神经发生。血管生成素-1（Ang 1）是胚胎和出生后生理和病理性血管生成的重要调节因子。虽然Ang 1可以保护外周血管系统免受缺血性损伤后的血管渗漏，但Ang 1在缺血性卒中后长期神经恢复中的作用仍然是难以捉摸的。本研究的目的是检查是否血管生成素1过表达通过慢病毒介导的基因转移增强神经血管重塑和改善功能的结果，在大鼠局灶性脑缺血模型。我们的研究结果表明，慢病毒介导的Ang 1基因转移导致改善神经行为和减少梗死体积，并保护缺血大鼠的血脑屏障（BBB）渗漏。此外，我们还发现Ang 1的这些作用与Ang 1增加血管密度和加速内源性神经元分化的能力有关。这些结果表明，血管生成素1是一种有前途的药物，用于治疗脑缺血。(C)2014年IBRO。由Elsevier Ltd.出版。保留所有权利。
Neuropathologic processes such as cerebral ischemia can enhance neurogenesis. Angiopoietin-1 (Ang1) emerges as a critical regulator of physiological and pathological angiogenesis during embryonic and postnatal life. Although Ang1 could protect peripheral vasculature from vascular leakage following ischemic injury, the role of Ang1 in long-term neurological recovery after ischemic stroke remains elusive. This study aims to examine whether Ang1 overexpression via lentivirus-mediated gene transfer enhances neurovascular remodeling and improves functional outcome in a rat model of focal cerebral ischemia. Our results demonstrated that lentivirus-mediated Ang1 gene transfer led to improved neurological behavior and reduced infarction volume, and protected against blood-brain barrier (BBB) leakage in the ischemic rats. In addition, we revealed that these effects of Ang1 are related to the ability of Ang1 to increase vascular density and accelerate endogenous neuronal differentiation. These findings suggest that Ang1 is a promising agent for the treatment of cerebral ischemia. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.