Abstract: Objective To investigate the relationship between Wnt signaling pathway and hypoxia -induced fractalkine expression in human umbilical vein endothelial cells. Methods HUVECs were cultivated and divided into three groups randomly (control group, hypoxia/reoxygenation group, LiCl 10mmol/L group), which were used to establish the hypoxia/reoxygenation models. The mRNA expressions of fractalkine and GSK-3β were assessed by RT-PCR. The intracellular distribution and expression of fractalkine were determined by immunofluorescent staining. The expression of GSK-3β and β-catenin were analyzed with immunocytochemistry. Results Compared with control group, in hypoxia/reoxygenation group, the expression of GSK-3β and β-catenin were increased (P<0.05), the mRNA and protein expression of fractalkine increased remarkably (P<0.05). Compared with hypoxia/reoxygenation group, in LiCl groups, the mRNA and protein expression of fractalkine reduced significantly (P<0.05), the expression of GSK-3β reduced but β-catenin increased relativitily (P<0.05). However, the mRNA expression of GSK-3β had no statistically difference in all groups. Conclusion The hypoxia induced the damage of HUVECs through upregulating fractalkine expression. LiCl pretreatment inhibited fractalkine expression proportional. Its mechanism may be related to the activation of Wnt signaling pathway.

Key words: hypoxia/reoxygenation, human umbilical vein endothelial cells, fractalkine, Wnt signaling pathway