Altered subcellular distribution of cadherin-5 in endothelial cells causedby the serum of pre-eclamptic patients

The main clinical features of pre-eclampsia are oedema and vascular leakage . Cadherin-5 mediates endothelial cell-cell contact in the vascular endothe lium end may regulate permeability as a vascular function. Therefore, we ad dressed the question of whether pre-eclampsia alters cadherin-5 expression and intracellular distribution. Confluent human umbilical vein endothelial cells (HUVEC) were incubated with 20% serum from patients with pre-eclampsi a (n = 18), haemolysis-elevated liver enzymes-low platelet syndrome (HELLP) (n = 12), pregnancy-induced hypertension (PIH) (n = 18) or normal pregnanc y (n = 10). After incubation with sera from patients with pre-eclampsia, im munostaining analyses showed cadherin-5 accumulation in vesicular and tubul ar structures of the Golgi apparatus. Immunoblot analyses of HUVEC after pr e-eclampsia serum incubation showed an increase of the stable form of cadhe rin-5 while degradation products decreased. Degradation of cadherin-5 takes place at the cell membrane, so this decrease may be due to a decrease of c adherin-5 in the cell membrane. The accumulation of cadherin-5 in the vesic ular and tubular structures of the Golgi apparatus indicates that targeting of cadherin-5 to the plasma membrane could be disrupted. We suggest that i ntracellular retention of cadherin-5 caused by serum factors in patients wi th pre-eclampsia may decrease the number of adhesion complexes in the cell membrane, thereby contributing to endothelial dysfunction.