l been defined that angiotensin II derived from the activated renin angiotensin system plays a key role in the regulation of cardiovascular homeostasis through its two receptors, Ang II type 1 and type 2 receptors, which maintain arter ial blood pressure, fluid and electrolyte homeostasis. Through the AT2 receptor, Ang II evokes vasodilatation, sodium excretion and blood pressure reduction, and thereby counteracts the effects of AT1 receptor. However, increasing evidence suggests that Ang II is also involved in tumor cell migration invasion, angiogenesis and metastasis through AT1 receptor during the tumor development. In patient with EOC, it has previ ously been reported that Ang II enhances vascular endo thelial growth factor secretion, angiogenesis and tumor cell invasion via up regulating G protein coupled AT1 receptor, importantly, angiogenesis and peritoneal dissemination of the EOC can selectively be blocked using AT1 receptor antagonist.

Therefore, consider able effort has been placed on the development of Ang II blockade therapy as a new strategy for EOC treatment. Recent studies have demonstrated that agonistic auto antibodies against type 1 angiotensin II receptor detected in preeclampsia induces significant placental trophoblast invasion, suggesting that PTC-209 HBr availability AT1 AA is one of the potential causative factors in development of pre eclampsia. We have previously reported that AT1 AA con stricts human fetoplacental blood vessels and restricts fetal perfusion through activating Ang II AT1 receptor.

Although animals studies have shown that activation of AT1 AA is associated with elevation of intracellular Ca2 in vascular smooth muscle cells, stimulation of pla cental and vascular NADPH oxidase and activation of NFB, all of which may cause inflammation and con tribute to pathogenesis of preeclampsia via AT1 AA, there {the full report| selleck chemical|selelck kinase inhibitor|selelck kinase inhibitor|buy ML323 is less specific data to show whether AT1 AA is elevated in patient with EOC and correlated with the advanced progression of EOC. Therefore, in the current study, we examined the serum AT1 AA titer in EOC patients and determined whether change in AT1 AA level is associated with malignant grades and angiogenic factor, VEGF. Using AT1 AA purified from EOC patients, we demonstrated the effects of AT1 AA on migration of ovarian cancer cells and microvascular density of chick embryo chorioallantoic membrane.

Furthermore, we investigated whether the AT1 AA elicited biological effects could be suppressed by autoantibody neutralizing AT1 AA peptide, and whether cell migration and angiogenesis stimulated by AT1 AA could be blocked by Ang II AT1 receptor antagonist. Methods Patients The study included 89 malignant EOC patients who were diagnosed and operated in the third hospital of Capital Medical University during the period of 05 2010 to 04 2012