TY - JOUR
T1 - Nitric oxide inhibits migration of cultured endothelial cells
AU - Lau, Ying Tung
AU - Ma, Wei Ching
PY - 1996/4/25
Y1 - 1996/4/25
N2 - 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 anitmigratory 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.
AB - 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 anitmigratory 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.
UR - http://www.scopus.com/inward/record.url?scp=0029882923&partnerID=8YFLogxK
U2 - 10.1006/bbrc.1996.0654
DO - 10.1006/bbrc.1996.0654
M3 - 文章
C2 - 8630019
AN - SCOPUS:0029882923
SN - 0006-291X
VL - 221
SP - 670
EP - 674
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -