摘要
血管内皮屏障功能的调节机制相当复杂。α┐凝血酶等炎性介质引起内皮通透性增高的机制可能是通过Ｇ蛋白激活磷脂酶，介导三磷酸肌醇等第二信使产生，并进一步激活蛋白激酶Ｃ和肌球蛋白轻链激酶，最终引起肌球蛋白轻链磷酸化，从而导致内皮细胞Ｆ┐肌动蛋白骨架重排，中心张力增加，细胞间裂隙形成。
The regulatory mechanisms of vascular endothelial barrier function are complicated. Inflammatory mediators, such as αthrombin, activate phospholipases to mediate generation of IP3 and other second messengers through receptorcoupled G protein. Protein kinase C and myosin light chain kinase are then activated, leading to phosphorylation of myosin light chains, rearrangement of Factin skeleton, interendothelial cell gap formation and increased endothelial permeability.
出处
《生理科学进展》
CAS
CSCD
北大核心
1998年第3期215-220,共6页
Progress in Physiological Sciences
关键词
屏障功能
内皮
通透性
调节
血管内皮
Barrier function
Endothelium
Permeablity
Regulation
