[Effects of inhibitors of intracellular signal transduction on lipopolysaccharide-induced increase in permeability of cultured pulmonary endothelial cell monolayers].
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.
Yonemaru
M
M
First Department of Medicine, Tokyo Medical College, Japan.
Kiyokawa
H
H
Kasuga
I
I
Minemura
K
K
Utsumi
K
K
Torii
Y
Y
Ichinose
Y
Y
Toyama
K
K
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*
D000418:Albumins; D008070:Lipopolysaccharides; D011493:Protein Kinase C