4-hydroxy-2-nonenal and diphenyleneiodonium

4-hydroxy-2-nonenal has been researched along with diphenyleneiodonium* in 1 studies

Other Studies

1 other study(ies) available for 4-hydroxy-2-nonenal and diphenyleneiodonium

Article	Year
Lysophosphatidylcholine is a major contributor to the synergistic effect of mildly oxidized low-density lipoprotein with endothelin-1 on vascular smooth muscle cell proliferation. Journal of cardiovascular pharmacology, 2002, Volume: 39, Issue:3 Endothelin-1 (ET-1) and oxidized low-density lipoprotein (ox-LDL) are associated with atherosclerosis and essential hypertension. We assessed the effect of mildly oxidized LDL (mox-LDL) and ox-LDL and their major oxidative components, i.e., reactive oxygen species (ROS), lysophosphatidylcholine (LPC), and 4-hydroxy-2-nonenal (HNE) and their interaction with ET-1 on vascular smooth muscle cell (VSMC) proliferation. Growth-arrested VSMCs isolated from the rabbit aorta were incubated with different concentrations of LDL, mox-LDL, ox-LDL, hydrogen peroxide (H(2)O(2)) (a donor of ROS), LPC, or HNE with or without ET-1. DNA synthesis in VSMCs was measured by [(3)H] thymidine incorporation. Mox-LDL, ox-LDL, H(2)O(2), LPC, HNE, or ET-1 stimulated DNA synthesis in a dose-dependent manner. Maximal effect was observed at 5 microg/ml for mox-LDL (162%) or ox-LDL (154%), 15 microM LPC (156%), 5 microM H2O2 (177%), 1 microM HNE (144%), and 0.1 microM ET-1 (195%). By contrast, LDL was without any significant effect. When added together, there was no synergistic effect of LDL, H2O2, or HNE with ET-1 on DNA synthesis. However, the effect of mox-LDL (0.1 microg/ml), ox-LDL (0.5 microg/ml), or LPC (10 microM) was potentiated by ET-1 (114%-338%, 133%-425%, 118%-333%, respectively). The mitogenic effect of mox-LDL, ox-LDL, or LPC and their interaction with ET-1 were inhibited by defatted albumin (10 microg/ml), antioxidant N-acetylcysteine (400 microM), the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (1 microM). The ET(A/B) receptor antagonist TAK044 (1 microM) or the MAPK kinase inhibitor PD098059 (10 microM) inhibited the mitogenic effect of ET-1 and its interaction with mox-LDL, ox-LDL, or LPC. The synergistic interaction of mox-LDL, ox-LDL, or LPC with ET-1 was completely reversed by the combined use of N-acetylcysteine and TAK044. Our results suggest that mox-LDL, ox-LDL, and their major phospholipid component LPC act synergistically with ET-1 in inducing VSMC proliferation by way of the activation of redox-sensitive and MAPK pathways. Topics: Acetylcysteine; Aldehydes; Animals; Aorta, Thoracic; Cell Count; Cell Division; Cells, Cultured; DNA; Endothelin Receptor Antagonists; Endothelin-1; Flavonoids; Free Radical Scavengers; Growth Inhibitors; Hydrogen Peroxide; Lipoproteins, LDL; Lysophosphatidylcholines; Male; Mitogen-Activated Protein Kinase Kinases; Muscle, Smooth, Vascular; NADPH Oxidases; Onium Compounds; Oxidants; Peptides, Cyclic; Rabbits; Reactive Oxygen Species	2002

Article

Year

Lysophosphatidylcholine is a major contributor to the synergistic effect of mildly oxidized low-density lipoprotein with endothelin-1 on vascular smooth muscle cell proliferation.

Journal of cardiovascular pharmacology, 2002, Volume: 39, Issue:3

Endothelin-1 (ET-1) and oxidized low-density lipoprotein (ox-LDL) are associated with atherosclerosis and essential hypertension. We assessed the effect of mildly oxidized LDL (mox-LDL) and ox-LDL and their major oxidative components, i.e., reactive oxygen species (ROS), lysophosphatidylcholine (LPC), and 4-hydroxy-2-nonenal (HNE) and their interaction with ET-1 on vascular smooth muscle cell (VSMC) proliferation. Growth-arrested VSMCs isolated from the rabbit aorta were incubated with different concentrations of LDL, mox-LDL, ox-LDL, hydrogen peroxide (H(2)O(2)) (a donor of ROS), LPC, or HNE with or without ET-1. DNA synthesis in VSMCs was measured by [(3)H] thymidine incorporation. Mox-LDL, ox-LDL, H(2)O(2), LPC, HNE, or ET-1 stimulated DNA synthesis in a dose-dependent manner. Maximal effect was observed at 5 microg/ml for mox-LDL (162%) or ox-LDL (154%), 15 microM LPC (156%), 5 microM H2O2 (177%), 1 microM HNE (144%), and 0.1 microM ET-1 (195%). By contrast, LDL was without any significant effect. When added together, there was no synergistic effect of LDL, H2O2, or HNE with ET-1 on DNA synthesis. However, the effect of mox-LDL (0.1 microg/ml), ox-LDL (0.5 microg/ml), or LPC (10 microM) was potentiated by ET-1 (114%-338%, 133%-425%, 118%-333%, respectively). The mitogenic effect of mox-LDL, ox-LDL, or LPC and their interaction with ET-1 were inhibited by defatted albumin (10 microg/ml), antioxidant N-acetylcysteine (400 microM), the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (1 microM). The ET(A/B) receptor antagonist TAK044 (1 microM) or the MAPK kinase inhibitor PD098059 (10 microM) inhibited the mitogenic effect of ET-1 and its interaction with mox-LDL, ox-LDL, or LPC. The synergistic interaction of mox-LDL, ox-LDL, or LPC with ET-1 was completely reversed by the combined use of N-acetylcysteine and TAK044. Our results suggest that mox-LDL, ox-LDL, and their major phospholipid component LPC act synergistically with ET-1 in inducing VSMC proliferation by way of the activation of redox-sensitive and MAPK pathways.

Topics: Acetylcysteine; Aldehydes; Animals; Aorta, Thoracic; Cell Count; Cell Division; Cells, Cultured; DNA; Endothelin Receptor Antagonists; Endothelin-1; Flavonoids; Free Radical Scavengers; Growth Inhibitors; Hydrogen Peroxide; Lipoproteins, LDL; Lysophosphatidylcholines; Male; Mitogen-Activated Protein Kinase Kinases; Muscle, Smooth, Vascular; NADPH Oxidases; Onium Compounds; Oxidants; Peptides, Cyclic; Rabbits; Reactive Oxygen Species

2002