Compounds > 15-hydroxy-5-8-11-13-eicosatetraenoic-acid

15-hydroxy-5-8-11-13-eicosatetraenoic-acid and thiazolyl-blue

15-hydroxy-5-8-11-13-eicosatetraenoic-acid has been researched along with thiazolyl-blue* in 1 studies

Other Studies

1 other study(ies) available for 15-hydroxy-5-8-11-13-eicosatetraenoic-acid and thiazolyl-blue

Article	Year
15-HETE suppresses K(+) channel activity and inhibits apoptosis in pulmonary artery smooth muscle cells. Apoptosis : an international journal on programmed cell death, 2009, Volume: 14, Issue:1 15-Hydroxyeicosatetraenoic acid (15-HETE) is an important hypoxic product from arachidonic acid (AA) in the wall of pulmonary vessels. Although its effects on pulmonary artery constriction are well known, it remains unclear whether 15-HETE acts on the apoptotic responses in pulmonary artery smooth muscle cells (PASMCs) and whether K(+) channels participate in this process. These hypothesises were validated by cell viability assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling, mitochondrial potentials assay, caspase activity assay and western blot. We found that 15-HETE enhanced cell survival, suppressed the expression and activity of caspase-3, upregulated bcl-2 and attenuated mitochondrial depolarization, prevented chromatin condensation and partly reversed K(+) channel opener-induced apoptosis in PASMCs under serum-deprived conditions. Our data indicated that 15-HETE inhibits the apoptosis in PASMCs through, at least in part, inactivating K(+) channels. Topics: Apoptosis; Arachidonic Acid; Caspase 3; Humans; Hydrogen Peroxide; Hydroxyeicosatetraenoic Acids; Hypoxia; Mitochondria; Models, Biological; Myocytes, Smooth Muscle; Potassium; Potassium Channels; Proto-Oncogene Proteins c-bcl-2; Pulmonary Artery; Tetrazolium Salts; Thiazoles	2009

Article

Year

15-HETE suppresses K(+) channel activity and inhibits apoptosis in pulmonary artery smooth muscle cells.

Apoptosis : an international journal on programmed cell death, 2009, Volume: 14, Issue:1

15-Hydroxyeicosatetraenoic acid (15-HETE) is an important hypoxic product from arachidonic acid (AA) in the wall of pulmonary vessels. Although its effects on pulmonary artery constriction are well known, it remains unclear whether 15-HETE acts on the apoptotic responses in pulmonary artery smooth muscle cells (PASMCs) and whether K(+) channels participate in this process. These hypothesises were validated by cell viability assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling, mitochondrial potentials assay, caspase activity assay and western blot. We found that 15-HETE enhanced cell survival, suppressed the expression and activity of caspase-3, upregulated bcl-2 and attenuated mitochondrial depolarization, prevented chromatin condensation and partly reversed K(+) channel opener-induced apoptosis in PASMCs under serum-deprived conditions. Our data indicated that 15-HETE inhibits the apoptosis in PASMCs through, at least in part, inactivating K(+) channels.

Topics: Apoptosis; Arachidonic Acid; Caspase 3; Humans; Hydrogen Peroxide; Hydroxyeicosatetraenoic Acids; Hypoxia; Mitochondria; Models, Biological; Myocytes, Smooth Muscle; Potassium; Potassium Channels; Proto-Oncogene Proteins c-bcl-2; Pulmonary Artery; Tetrazolium Salts; Thiazoles

2009