Structural mechanisms in the abolishment of VEGF-induced microvascular hyperpermeability by cAMP.
Structural mechanisms in the abolishment of VEGF-induced microvascular hyperpermeability by cAMP.
复制标题
cAMP 消除 VEGF 诱导的微血管通透性过高的结构机制。
DOI：
10.1115/1.2187047
复制
发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Chen,Bin
中科院分区：
文献类型：
--
作者：
Fu,BingmeiM;Shen,Shang;Chen,Bin
为了研究内皮内 cAMP 水平升高消除或减弱血管内皮生长因子 (VEGF) 引起的微血管通透性短暂增加的结构机制，我们检查了 cAMP 对 VEGF 诱导的小溶质荧光素钠 (Stokes)、中等大小溶质乳清蛋白 (Stokes) 和大溶质通透性过高的影响。 白蛋白（BSA，Stokes）在单独灌注的青蛙肠系膜微血管上。在cAMP类似物、8-溴-cAMP预处理后，在(从单独使用VEGF的对照倍数峰值增加到用VEGF和cAMP对照倍数)、(从单独使用VEGF对照倍数峰值增加到用VEGF和cAMP对照倍数峰值增加)和(从单独用VEGF对照倍数峰值增加到用VEGF和cAMP对照峰值增加)中，VEGF的初始增加被完全消除。根据这些测量数据，我们的数学模型预测表明，形成微血管壁的内皮细胞之间的间隙中紧密连接链数量的增加是cAMP消除VEGF诱导的通透性过高的机制之一。
To investigate the structural mechanisms by which elevation of the intraendothelial cAMP levels abolishes or attenuates the transient increase in microvascular permeability by vascular endothelial growth factor (VEGF), we examined cAMP effect on VEGF-induced hyperpermeability to small solute sodium fluorescein (Stokes), intermediate-sized solute-lactalbumin (Stokes), and large solute albumin (BSA, Stokes)on individually perfused microvessels of frog mesenteries. Afterpretreatment ofcAMP analog, 8-bromo-cAMP, the initial increase byVEGF was completely abolished in(from a peak increase oftimes control with VEGF alone totimes control with VEGF and cAMP), in(from a peak increase oftimes control with VEGF alone totimes control with VEGF and cAMP), and in(from a peak increase oftimes control with VEGF alone totimes control with VEGF and cAMP). Based on these measured data, the prediction from our mathematical models suggested that the increase in the number of tight junction strands in the cleft between endothelial cells forming the microvessel wall is one of the mechanisms for the abolishment of VEGF-induced hyperpermeability by cAMP.