stemphone and rottlerin

stemphone has been researched along with rottlerin* in 1 studies

Other Studies

1 other study(ies) available for stemphone and rottlerin

Article	Year
High-glucose-altered endothelial cell function involves both disruption of cell-to-cell connection and enhancement of force development. The Journal of pharmacology and experimental therapeutics, 2006, Volume: 318, Issue:2 Vascular endothelial cells (ECs), which regulate vascular tonus, serve as a barrier at the interface of vascular tissue. It is generally believed that alteration of this barrier is correlated with diabetic complications; however, a detailed mechanism has not been elucidated. This study examined alteration of bovine arterial EC functions stimulated by a thromboxane A2 analog (9,11-dideoxy-11 alpha,9 alpha-epoxymethano prostaglandin F(2 alpha); U46619) under normal and high-glucose (HG) conditions. U46619 treatment increased EC layer permeability in a time- and dose-dependent fashion. This response initially disrupted calcium-dependent EC-to-EC connections, namely, vascular endothelial cadherin (VE-CaD). Thereafter, EC force development in association with morphological changes was detected employing a reconstituted EC fiber technique, resulting in paracellular hole formation in the EC layer. Thus, we confirmed that U46619-induced enhancement of EC layer permeability involves these sequential steps. Similar trials were performed using a concentration twice that of normal glucose (22.2 mM glucose for 48 h). This treatment significantly enhanced U46619-induced EC layer permeability; furthermore, increases in both rate of VE-CaD disruption and EC fiber contraction were evident. Inhibition of calcium-independent protein kinase C and diacylglycerol kinase indicated that the glucose-dependent increase in VE-CaD disruption was mediated by a calcium-independent mechanism. Moreover, EC contraction was regulated by a typical calcium-independent pathway associated with rho kinase and actin stress fiber. Contraction was also enhanced under HG conditions. This investigation revealed that glucose-dependent enhancement of EC layer permeability is related to increases in VE-CaD disruption and EC contraction. Increases in both parameters were mediated by alteration of a calcium-independent pathway. Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Acetophenones; Animals; Benzopyrans; Benzoquinones; Cadherins; Calcium; Capillary Permeability; Cattle; Cell Communication; Cells, Cultured; Egtazic Acid; Endothelial Cells; Enzyme Inhibitors; Extracellular Space; Glucose; Image Processing, Computer-Assisted; Immunohistochemistry; Isometric Contraction; Muscle Contraction; Muscle, Smooth, Vascular; Vasoconstrictor Agents	2006

Article

Year

High-glucose-altered endothelial cell function involves both disruption of cell-to-cell connection and enhancement of force development.

The Journal of pharmacology and experimental therapeutics, 2006, Volume: 318, Issue:2

Vascular endothelial cells (ECs), which regulate vascular tonus, serve as a barrier at the interface of vascular tissue. It is generally believed that alteration of this barrier is correlated with diabetic complications; however, a detailed mechanism has not been elucidated. This study examined alteration of bovine arterial EC functions stimulated by a thromboxane A2 analog (9,11-dideoxy-11 alpha,9 alpha-epoxymethano prostaglandin F(2 alpha); U46619) under normal and high-glucose (HG) conditions. U46619 treatment increased EC layer permeability in a time- and dose-dependent fashion. This response initially disrupted calcium-dependent EC-to-EC connections, namely, vascular endothelial cadherin (VE-CaD). Thereafter, EC force development in association with morphological changes was detected employing a reconstituted EC fiber technique, resulting in paracellular hole formation in the EC layer. Thus, we confirmed that U46619-induced enhancement of EC layer permeability involves these sequential steps. Similar trials were performed using a concentration twice that of normal glucose (22.2 mM glucose for 48 h). This treatment significantly enhanced U46619-induced EC layer permeability; furthermore, increases in both rate of VE-CaD disruption and EC fiber contraction were evident. Inhibition of calcium-independent protein kinase C and diacylglycerol kinase indicated that the glucose-dependent increase in VE-CaD disruption was mediated by a calcium-independent mechanism. Moreover, EC contraction was regulated by a typical calcium-independent pathway associated with rho kinase and actin stress fiber. Contraction was also enhanced under HG conditions. This investigation revealed that glucose-dependent enhancement of EC layer permeability is related to increases in VE-CaD disruption and EC contraction. Increases in both parameters were mediated by alteration of a calcium-independent pathway.

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Acetophenones; Animals; Benzopyrans; Benzoquinones; Cadherins; Calcium; Capillary Permeability; Cattle; Cell Communication; Cells, Cultured; Egtazic Acid; Endothelial Cells; Enzyme Inhibitors; Extracellular Space; Glucose; Image Processing, Computer-Assisted; Immunohistochemistry; Isometric Contraction; Muscle Contraction; Muscle, Smooth, Vascular; Vasoconstrictor Agents

2006