Research on inhibitory effect of celecoxib against migration of vascular endothelial cells / 医学研究生学报

ABSTRACT

Objective The mechanism of celecoxib in influencing the migration of vascular endothelial cells is still not clear.The aim of this study was to investigate the effect of celecoxib against migration of vascular endothelial cells and its mechanism.Methods Human umbilical vein endothelial cells (HUVECs) were obtained from the cell bank of Central Laboratory of Nanjing General Hospital of Nanjing Military Command.Transwell was used to measure the migration rate of HUVECs after the administration of 0μmol/L, 10μmol/L and 20μmol/L celecoxib.Immunofluorescence, western blot, and qRT-PCR were used to detect protein and mRNA expression of COX-2 and PTPRJ in HUVECs.Results The expression of COX-2, PTPRJ in HUVECs were detected by immunofluorescence.After the administration of 20μmol/L, 10μmol/L and 0μmol/L celecoxib, HUVEC migration rate was (12.35±3.61), (32.80±5.92) and (63.15±5.83) respectively, representing significant difference (P<0.01).COX-2 protein expression in 20μmol/L group (0.16±0.03) and 10μmol/L group (0.36±0.05) decreased significantly compared with that of 0μmol/L group (0.77±0.07) (P<0.01).Moreover, COX-2 protein expression in 20μmol/L group significantly decreased compared with that of 10μmol/L group(P<0.05).PTPRJ protein expression in 20μmol/L group (0.82±0.05) and 10μmol/L group (0.51±0.02) was respectively higher than that of 0μmol/L group (0.27±0.04) (P<0.01).Moreover, PTPRJ protein expression in 20μmol/L group significantly increased compared with that of 10μmol/L group (P<0.05).COX-2 mRNA expression in 20μmol/L group (0.06±0.02) and 10μmol/L group (0.22±0.05) decreased significantly compared with that of 0μmol/L group (1.05±0.13) (P<0.01).PTPRJ mRNA expression in 20μmol/L group (60.27±11.31) and 10μmol/L group (16.50±3.18) increased significantly compared with that of 0μmol/L group (0.99±0.25) (P<0.01).Conclusion Celecoxib inhibits the migration of vascular endothelial cells, which may be related to the inhibition of COX-2 expression and the up-regulation of PTPRJ expression in vascular endothelial cells.