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局灶性脑缺血后 Src、SSeCKS 和血管生成因子的时间进程:与血管生成和脑水肿的相关性。

Temporal profile of Src, SSeCKS, and angiogenic factors after focal cerebral ischemia: correlations with angiogenesis and cerebral edema.

机构信息

Department of Pathology, First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, PR China.

出版信息

Neurochem Int. 2011 Jul;58(8):872-9. doi: 10.1016/j.neuint.2011.02.014. Epub 2011 Feb 18.

Abstract

A better understanding of the underlying mechanisms of angiogenesis and vascular permeability is necessary for the development of therapeutic strategies for ischemic injury. The purpose of this study was to examine the spatial and temporal expression of Src and Src-suppressed C kinase substrate (SSeCKS) in brain after middle cerebral artery occlusion (MCAO) and elucidate the relationships among Src, SSeCKS, and the key angiogenic factors present after stroke. Rats were subjected to either MCAO or sham operation. Reverse transcriptase-polymerase chain reaction and Western blotting results revealed that Src gradually increased starting as early as 2 h after MCAO and remained high for 1 day. In contrast, SSeCKS decreased after MCAO. Src expression correlated positively with that of vascular endothelial growth factor and angiopoietin-2, and negatively with that of SSeCKS, angiopoietin-1, and zonula occludens-1. However, SSeCKS had the reverse correlations. Changes in the expression of these factors correlated with the progress of angiogenesis and cerebral edema. Dynamic temporal changes in Src and SSeCKS expression may modulate angiogenesis and cerebral edema formation after focal cerebral ischemia.

摘要

为了开发治疗缺血性损伤的策略,需要更好地了解血管生成和血管通透性的潜在机制。本研究的目的是研究大脑中脑动脉闭塞(MCAO)后Src 和 Src 抑制 C 激酶底物(SSeCKS)的时空表达,并阐明 Src、SSeCKS 与中风后存在的关键血管生成因子之间的关系。大鼠接受 MCAO 或假手术。逆转录聚合酶链反应和 Western blot 结果表明,Src 从 MCAO 后 2 小时开始逐渐增加,并持续高表达 1 天。相比之下,SSeCKS 在 MCAO 后减少。Src 的表达与血管内皮生长因子和血管生成素-2 的表达呈正相关,与 SSeCKS、血管生成素-1 和封闭蛋白-1 的表达呈负相关。然而,SSeCKS 则呈相反的相关性。这些因子表达的变化与血管生成和脑水肿的进展相关。Src 和 SSeCKS 表达的动态时间变化可能调节局灶性脑缺血后的血管生成和脑水肿形成。

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