TY - JOUR
T1 - The beneficial effect of taurine on the prevention of human endothelial cell death
AU - Wang, Jiang Huai
AU - Redmond, H. Paul
AU - Watson, R. William G.
AU - Condron, Claire
AU - Bouchier-Hayes, David
PY - 1996/11
Y1 - 1996/11
N2 - This study was designed to test the hypothesis that the antioxidant taurine may modulate human endothelial cell (EC) death (apoptosis versus necrosis). Sodium arsenite (80 μM) alone and in combination with tumor necrosis factor-α (25 ng/mL) caused EC apoptosis after 24 h of treatment. Taurine (.5 mg/mL) added at 0 and 6 h could significantly attenuate EC apoptosis, and maintain EC function as represented by increased intercellular adhesion molecule-1 expression and oxidative state in response to lipopolysaccharide and tumor necrosis factor-α stimulation. EC necrosis was induced by activated neutrophils (PMNs). Taurine reduced PMN-mediated EC necrosis in a dose-dependent manner. Moreover, treatment of ECs with a calcium ionophore, A23187 (1.0-4.0 μM), resulted in both EC apoptosis and necrosis. Taurine significantly abrogated A23187-mediated intracellular calcium elevation and EC death. These data indicate that taurine, possibly through its antioxidant activity and regulation of intracellular calcium flux, can prevent EC dysfunction and cell death, which may have implications for the application of this amino acid in the amelioration of acute lung injury during systemic inflammatory response syndrome.
AB - This study was designed to test the hypothesis that the antioxidant taurine may modulate human endothelial cell (EC) death (apoptosis versus necrosis). Sodium arsenite (80 μM) alone and in combination with tumor necrosis factor-α (25 ng/mL) caused EC apoptosis after 24 h of treatment. Taurine (.5 mg/mL) added at 0 and 6 h could significantly attenuate EC apoptosis, and maintain EC function as represented by increased intercellular adhesion molecule-1 expression and oxidative state in response to lipopolysaccharide and tumor necrosis factor-α stimulation. EC necrosis was induced by activated neutrophils (PMNs). Taurine reduced PMN-mediated EC necrosis in a dose-dependent manner. Moreover, treatment of ECs with a calcium ionophore, A23187 (1.0-4.0 μM), resulted in both EC apoptosis and necrosis. Taurine significantly abrogated A23187-mediated intracellular calcium elevation and EC death. These data indicate that taurine, possibly through its antioxidant activity and regulation of intracellular calcium flux, can prevent EC dysfunction and cell death, which may have implications for the application of this amino acid in the amelioration of acute lung injury during systemic inflammatory response syndrome.
UR - https://www.scopus.com/pages/publications/0030278223
U2 - 10.1097/00024382-199611000-00006
DO - 10.1097/00024382-199611000-00006
M3 - Article
C2 - 8946648
AN - SCOPUS:0030278223
SN - 1073-2322
VL - 6
SP - 331
EP - 338
JO - Shock
JF - Shock
IS - 5
ER -