NITRIC-OXIDE INHIBITS MIGRATION OF CULTURED ENDOTHELIAL-CELLS

Endothelial cell migration is an important event in both physiological and pathophysiological processes. Although nitric oxide (NO) plays a critical role in regulating vascular functions, it is not known whethe r NO modulates migration of endothelial cells. We show here that chemi cally-derived NO inhibited the serum-induced migration of cultured hum an umbilical vein endothelial cells (HUVEC) in a time- and dose-depend ent manner. The sensitivity of inhibition by S-nitroso-N-acetylpenicil lamine (SNAP, a NO donor) was 2.36+/-1.032x10(-4) M (n=4). This effect was attributed to NO since (1) other NO donor (e.g., sodium nitroprus side) also exhibited anitmigratory effect, (2) pre-incubated SNAP (72 h) had no effect, (3) hemoglobin, a NO scavenger, eliminated the effec t; while (4) superoxide dismutase, a NO protector, enhanced the antimi gratory effect. Furthermore, 8-bromo-cGMP also inhibited the serum-ind uced migration of HUVEC. These data appear to support the notion that NO may serve as an important signaling molecule for neovascularization . (C) 1996 Academic Press, Inc.