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 whether NO modulates migration of endothelial cells. We show here that chemically-derived NO inhibited the serum-induced migration of cultured human umbilical vein endothelial cells (HUVEC) in a time- and dose-dependent manner. The sensitivity of inhibition by S-nitroso-N-acetylpenicillamine (SNAP, a NO donor) was 2.36 +/- 1.032 x 10(-4) M (n = 4). This effect was attributed to NO since (1) other NO donor (e.g., sodium nitroprusside) also exhibited antimigratory effect, (2) pre-incubated SNAP (72 h) had no effect, (3) hemoglobin, a NO scavenger, eliminated the effect; while (4) superoxide dismutase, a NO protector, enhanced the antimigratory effect. Furthermore, 8-bromo-cGMP also inhibited the serum-induced migration of HUVEC. These data appear to support the notion that NO may serve as an important signaling molecule for neovascularization.