title: [Effects of inhibitors of intracellular signal transduction on lipopolysaccharide-induced increase in permeability of cultured pulmonary endothelial cell monolayers].
abstract: To investigate the mechanism of lipopolysaccharide (LPS)-induced endothelial response, we measured the permeability to albumin of cultured pulmonary endothelial cell monolayers. PMA and SC-9, used as activators for protein kinase C (PCK), failed to cause an increase in permeability to albumin. H-7, a potent PKC inhibitor, did not prevent the LPS-induced increase in permeability to albumin. In contrast, H-8, which strongly inhibits cyclic nucleotide-dependent protein kinases, and a calmodulin antagonist prevented the LPS-induced increase in permeability to albumin. These results suggest that calmodulin and protein kinases other than PCK are implicated in the mechanism of LPS-induced increase in permeability to albumin.
authors.affiliation: First Department of Medicine, Tokyo Medical College, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yonemaru
authors.forename: H
authors.initials: H
authors.lastname: Kiyokawa
authors.forename: I
authors.initials: I
authors.lastname: Kasuga
authors.forename: K
authors.initials: K
authors.lastname: Minemura
authors.forename: K
authors.initials: K
authors.lastname: Utsumi
authors.forename: Y
authors.initials: Y
authors.lastname: Torii
authors.forename: Y
authors.initials: Y
authors.lastname: Ichinose
authors.forename: K
authors.initials: K
authors.lastname: Toyama
mesh_terms: D000418:Albumins / Q000493:pharmacokinetics; D004727:Endothelium / Q000166:cytology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000166:cytology / Q000187:drug effects*; D010539:Permeability; D011493:Protein Kinase C / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D000418:Albumins; D008070:Lipopolysaccharides; D011493:Protein Kinase C