Increased intracellular calcium transients by calmodulin antagonists differentially modulate tumor necrosis factor-α-induced E-selectin and ICAM-1 expression
KH Chen, BHJ Chang, P Younan, SG Shlykov… - Atherosclerosis, 2002 - Elsevier
We investigated the role of intracellular calcium ([Ca2+] i) in adhesion molecule expression
in human umbilical vascular endothelial cells (HUVECs). Calmodulin (CaM) antagonists, W-
7, trifluoperazine and chlorpromazine, triggered a rise in [Ca2+] i in HUVECs. In the
presence of extracellular Ca2+, thapsigargin pretreatment completely prevented W-7-
stimulated increase in [Ca2+] i, indicating that increase is attributable to the release of Ca2+
from internal stores. The increased [Ca2+] i acted as a second messenger to enhance tumor …
in human umbilical vascular endothelial cells (HUVECs). Calmodulin (CaM) antagonists, W-
7, trifluoperazine and chlorpromazine, triggered a rise in [Ca2+] i in HUVECs. In the
presence of extracellular Ca2+, thapsigargin pretreatment completely prevented W-7-
stimulated increase in [Ca2+] i, indicating that increase is attributable to the release of Ca2+
from internal stores. The increased [Ca2+] i acted as a second messenger to enhance tumor …