Strey Anke, Janning Annette, Barth Holger, Gerke Volker
Institute of Medical Biochemistry, ZMBE, University of Münster, Münster, Germany.
FEBS Lett. 2002 Apr 24;517(1-3):261-6. doi: 10.1016/s0014-5793(02)02643-1.
Bacterial toxins affecting Rho activity in microvascular endothelial cells were employed to elucidate whether endothelial Rho participates in regulating the migration of monocytes across monolayers of cultured endothelial cells. Inactivation of Rho by the Clostridium C3 exoenzyme resulted in an increased adhesion of peripheral blood monocytes to the endothelium and a decreased rate of transendothelial monocyte migration. Cytotoxic necrotizing factor 1-mediated activation of endothelial Rho also reduced the rate of monocyte transmigration, but did not affect monocyte-endothelium adhesion. Thus, efficient leukocyte extravasation requires Rho signaling not only within the migrating leukocytes but also within the endothelial lining of the vessel wall.
利用影响微血管内皮细胞中Rho活性的细菌毒素,来阐明内皮Rho是否参与调节单核细胞穿过培养的内皮细胞单层的迁移过程。肉毒梭菌C3外切酶使Rho失活,导致外周血单核细胞与内皮的黏附增加,以及单核细胞跨内皮迁移速率降低。细胞毒性坏死因子1介导的内皮Rho激活也降低了单核细胞的迁移速率,但不影响单核细胞与内皮的黏附。因此,有效的白细胞渗出不仅需要迁移中的白细胞内的Rho信号,还需要血管壁内皮中的Rho信号。