中文摘要：

背景高 microvascular 渗透在多重疾病例如的病理学的过程起一个必要作用腐败吃惊，尖锐的肺损害和尖锐呼吸悲痛症候群，和 burns.Inhibiting hyperpermeability 为控制这些 conditions.Cdc42 是重要的作为小 Rho GTPase 家庭的一个主要成员，在控制并且调整 junctional permeability.We 试图产生并且识别 endothelial 的 endothelial 起一个关键作用由Cre/的特定的cdc42缺乏的老鼠在 F2 产生的cdc42Flox/FloxTie2Cre+/-老鼠是目标 mice.If 缺乏的老鼠没熬过的 cdc42 ，我们将观察 cdc42 缺乏的老鼠胚胎，并且把他们与野类型的老鼠 embryos.Results Cdc42Flox/+Cre+/-老鼠作比较带着 cdc42Flox/Flox 老鼠被交配，在生活后代之中，没有目标 mice.We 发现了在 E7.5-E16.5 stage.We 的缺乏的胚胎观察了的 endothelial 专辑 cdc42 的cdc42Flox/FloxCre+/-缺乏的胚胎多是的那 cdc42 更小的、有的 fe

英文摘要：

Background High microvascular permeability plays an essential role in pathological process of multiple diseases such as septic shock, acute lung injury and acute respiratory distress syndrome, and burns. Inhibiting hyperpermeability is significant for controlling these conditions. Cdc42, as a main member of the small Rho GTPase family, plays a critical role in controlling and regulating the endothelial junctional permeability. We aimed to generate and identify endothelial specific cdc42-deficient mice by the Cre/Ioxp recombination approach, for examination in an animal model of the contribution of the cdc42 gene in the microvascular barrier function. Methods We crossed cdc42^Flox/Flox mice with mice expressing endothelial cell-specific Cre recombinase, and the offspring with the genotype cdc42^FloX/＋Tie2Cre^＋/- were back-crossed with the cdc42^Flox/Flox mice. The cdc42^Flox/FloxTie2Cre^＋/- mice in the F2 generation were the target mice. If the cdc42 deficient mice did not survive, we would observe the cdc42 deficient mice embryos, and compare them with wild-type mice embryos. Results Cdc42^flox/＋Cre^＋/- mice were mated with the cdc42^Flox/Flox mice and among the living offspring there were no cdc42^Flox/FloCre^＋/- target mice. We found the endothelial special cdc42 deficient embryos at the E7.5-E16.5 stage. We observed that cdc42 deficient embryos were much smaller, had fewer vessels and were a little more swollen compared with the wild-type embryos. Conclusions Endothelial specific knockout of cdc42 caused embryonic lethality and the mice did not survive to birth. The target embryos were much smaller, had fewer vessels and were a little more swollen compared with the wild-type embryos. These results demonstrated that the cdc42 plays an important role in development of embryos and in development of microvessels as well as microvascular permeability.