Abstract: Objective To explore the roles of 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) in cigarette smoke extract (CSE)-induced change of human umbilical vein endothelial cells (HUVECs) migration. Methods To determine the migration and angiogenesis of HUVECs with“scratch assay” and capillary-like tube formation assay. To observe the expression of occludin with western blot. Results CSE significantly inhibits the migration of HUVECs. Cell number of wound closure in one visual field decreases from 629±28 in control to 364±17 in CSE group (P < 0.01). 15d-PGJ2 treatment increases the cell number of wound closure from 364±17 in CSE group to 546±20 in 15d-PGJ2+CSE group (P < 0.01). CSE inhibits the angiogenesis of HUVECs. 15d-PGJ2 could attenuate CSE-induced inhibition of HUVECs angiogenesis. The expression of occludin decreases from 0.37±0.04 in control to 0.12±0.03 in CSE group (P < 0.01) and increases to 0.28±0.04 in 15d-PGJ2+CSE group (P < 0.01 compared with CSE group), but still lower than control (P < 0.05). Conclusions CSE may inhibit the migration of HUVECs via down-regulation of occludin. 15d-PGJ2 could attenuate the change of occludin to rescue the HUVECs migration inhibited by CSE.

Key words: Cigarette smoke extract, Endothelial cell migration, 15d-PGJ2