Abstract
To find the key factors that were involved in the survival and vascular endothelial differentiation of chick blatodisc induced by fibroblast growth factor 2 (FGF‐2), we built a chick vasculogenesis model in vitro. Subsequently, the activities of phosphatidylcholine‐specific phospholipase C (PC‐PLC), including Ca^2+^‐dependent and ‐independent PC‐PLC, and the level of reactive oxygen species (ROS) were evaluated during the endothelial differentiation of chick blastodisc. The results showed that Ca^2+^‐indepentent PC‐PLC underwent a remarkable increase in 24 h (P < 0.01), then it decreased gradually with the cell differentiation, while the Ca^2+^‐depentent PC‐PLC was nearly not changed in the whole process. At the same time, ROS level dramatically decreased during the cell differentiation. To understand the role of PC‐PLC and how it performs its function in the vascular endothelial differentiation induced by FGF‐2, we suppressed PC‐PLC activity by its specific inhibitor D609 (tricyclodecan‐9‐yl potassium xanthate) at 24 h during the cell differentiation. As a result, the cell differentiation could not progress and the intracellular level of ROS was elevated. The data suggested that PC‐PLC and ROS were involved in chicken blastodisc differentiation to vascular endothelial cells. PC‐PLC was an important factor in the blastodisc cell survival and differentiation, and it might perform its function associated with ROS. J. Cell. Biochem. 102: 421–428, 2007. © 2007 Wiley‐Liss, Inc.