ULTRASTRUCTURE AND PERMEABILITY OF ENDOTHELIUM

内皮的超微结构和渗透性

• 批准号: 3343830
• 负责人: GIUSEPPE G PIETRA
• 金额: $ 18.35万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 1984
• 资助国家: 美国
• 起止时间: 1984-08-01 至 1995-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3343830
• 关键词: glycoproteins; hydrogen peroxide; immunocytochemistry; immunoelectron microscopy; laboratory rat; lung; lung disorder; microcirculation; morphology; oxidizing agents; phosphoproteins; pulmonary circulation; pulmonary edema; tight junctions; transmission electron microscopy; vascular endothelium; vascular endothelium permeability

This grant renewal is an extension of our studies on the structural determinants of vascular permeability in the lung. The long-range objective is to identify the components of the tight and adhering junctions which regulate the permeability barrier in the pulmonary endothelium. Although proteins specific for the two types of endothelial junctions have been recently identified, no information currently exists regarding their distribution in different segments of the pulmonary vasculature and their relationship to structure and function of the endothelial permeability barrier. Using colloidal gold techniques and antibodies, which recognize ZO-1 and Plakoglobin, two junction-specific proteins, we will determine, by morphometry and immuno electron microscopy, the distribution of these components of the endothelial junctional complex in various segments of the rat pulmonary vascular system. In a rat model of H202-induced pulmonary edema we will correlate increased endothelial permeability with selective loss of junctional components as detected by immuno electron microscopy and freeze-fracture techniques. These studies are expected to provide new insight in the pathogenesis of a variety of human pulmonary diseases such as the Adult Respiratory Distress Syndrome (ARDS), oxygen toxicity and ischemia-reperfusion injury in which oxygen derivatives and H202 in particular, are released by activated neutrophiles or endothelial cells.

这种赠款更新是我们关于结构的研究的扩展 肺中血管通透性的决定因素。 远程 目的是确定紧密而坚固的连接的组成部分 调节肺部内皮中的渗透性屏障。 尽管针对两种类型的内皮连接的蛋白质具有 最近被确定了，目前尚无有关其的信息 在肺脉管系统的不同部分中的分布及其 与内皮通透性的结构和功能的关系 障碍。 使用胶体金技术和抗体，识别 ZO-1和Plakoglobin，两种连接特异性蛋白，我们将通过 形态计量学和免疫电子显微镜，这些分布 内皮连接络合物的组成部分 大鼠肺血管系统。 在H202诱导的肺的大鼠模型中 水肿我们将增加内皮渗透性与选择性相关 通过免疫电子显微镜检测到的连接组件的损失和 冻结技术。 这些研究有望提供新的 洞察各种人类肺部疾病的发病机理 作为成人呼吸窘迫综合征（ARDS），氧毒性和 缺血再灌注损伤，其中氧衍生物和H202在 特别是活化的中性粒细胞或内皮细胞释放。