Angiotensin II stimulates intercellular adhesion molecule-1 via an AT1 receptor/nuclear factor-κB pathway in brain microvascular endothelial cells

摘要: Microvascular changes in the brain are significant causes of cerebral edema and ischemia injury. A number studies suggest that angiotensin (Ang) II may be involved initiation regulation processes occurring ischemia. We recently reported Ang injures microvascular endothelial cells (BMEC) partially via stimulating intercellular adhesion molecule-1 (ICAM-1) expression. However, signaling cascade leading to II-induced ICAM-1 expression BMEC was unclear. The present study tested hypothesis induces an AT1 receptor/nuclear factor-kappaB (NF-kappaB) pathway BMEC. directly stimulated mRNA protein primary cultured treatment also resulted degradation IkappaBalpha increase NF-kappaB p65 subunit nucleus as well DNA binding activity nuclear NF-kappaB. These effects were abolished by pretreatment with selective receptor antagonists, losartan compound EXP-2528, or plus AT2 antagonist PD123319, but not PD123319 alone. Moreover, there no differences between groups. findings indicate upregulation mediated receptor/NF-kappaB pathway.