BACKGROUND: @entity548 ( @entity548 )-induced @entity11924 involves disruption of endothelial cell adherens junctions leading to increase in paracellular permeability. b-Catenin, an integral component of the adherens junctional complex and Wnt pathway, and @entity4124 via its apoptotic signaling regulate endothelial cell barrier integrity. We have hypothesized that inhibiting phosphorylation of b-catenin and @entity4124 activity using glycogen synthase kinase 3-specific inhibitor @entity25650 would attenuate @entity11924 following @entity548 . METHODS: In @entity35 , @entity548 was induced by withdrawing blood to reduce mean arterial pressure to 40 mm Hg for 60 minutes followed by resuscitation. @entity35 were given @entity25650 (600  g/kg) intravenously 10 minutes before shock. To study microvascular permeability, the @entity35 were intravenously injected with @entity2822 ( @entity2823 )-albumin (50 mg/kg), and its flux across the mesenteric postcapillary venules was determined using intravital microscopy. In cell culture studies, @entity35 lung microvascular endothelial cell monolayers grown on Transwell plates were pretreated with @entity25650 (5  M) followed by BAK (5  g/mL) and @entity4124 (5  g/mL) protein transfection. @entity2823 -albumin (5 mg/mL) flux across cell monolayers indicates change in monolayer permeability. Activity of canonical Wnt pathway was determined by luciferase assay. @entity4124 enzyme activity was assayed fluorometrically. RESULTS: The @entity548 group showed significant increase in @entity2823 -albumin extravasation (p < 0.05) compared with sham. @entity25650 significantly decrease @entity548 -induced @entity2823 -albumin extravasation (p < 0.05). Pretreatment with @entity25650 protected against a BAK-induced increase in @entity35 lung microvascular endothelial cell monolayer permeability and @entity4124 activity but failed to show similar results with a @entity4124 -induced increase in monolayer permeability. @entity6035 treatment showed an increase in b-catenin-dependent T-cell factor-mediated transcription. CONCLUSION: Inhibiting phosphorylation of b-catenin and @entity4124 activity using glycogen synthase kinase 3-specific inhibitor @entity25650 help regulates @entity548 -induced @entity11924 .

Glycogen synthase kinase 3 inhibitor protects against @entity11924 following XXXX .

@entity548 :: ('MESH:D006470', 'Disease') :: ['Hemorrhagic shock', 'HS'] @entity35 :: ('10116', 'Species') :: ['rat', 'Sprague-Dawley rats', 'Rats', 'rats'] @entity6035 :: ('303181(Tax:10116)', 'Gene') :: ['Wnt3a'] @entity2822 :: ('CHEBI:37926', 'Chemical') :: ['fluorescein isothiocyanate'] @entity2823 :: ('MESH:D016650', 'Chemical') :: ['FITC'] @entity11924 :: ('MESH:D017566', 'Disease') :: ['microvascular hyperpermeability'] @entity25650 :: ('MESH:C417521', 'Chemical') :: ['SB216763'] @entity4124 :: ('25402(Tax:10116)', 'Gene') :: ['caspase 3', 'Caspase 3']
@entity548 :: (MESH:D006470,Disease) :: ['hemorrhagic shock']
