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.
Lau
Y T
YT
Department of Physiology, Chang Gung College of Medicine and Technology, Taoyuan, Taiwan, ROC.
Ma
W C
WC
D002465:Cell Movement / Q000187:drug effects*; D002478:Cells, Cultured; D006152:Cyclic GMP / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D009569:Nitric Oxide / Q000494:pharmacology*; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D026423:S-Nitroso-N-Acetylpenicillamine
D009569:Nitric Oxide; D026423:S-Nitroso-N-Acetylpenicillamine; D010396:Penicillamine; D006152:Cyclic GMP