PMID: 9424406Mar 1, 1997Paper

Protein kinase inhibitor attenuates an increase in endothelial monolayer permeability induced by tumour necrosis factor-alpha

Respirology : Official Journal of the Asian Pacific Society of Respirology
M YonemaruK Toyama

Abstract

We questioned the mechanism of the increase in pulmonary endothelial permeability induced by tumour necrosis factor-alpha (TNF-alpha), a cytokine implicated in the pathogenesis of adult respiratory distress syndrome. As a measure of permeability, we determined the albumin transferred across cultured pulmonary endothelial monolayers prepared on a porous filter. The agents evaluated included protein kinase inhibitors H-7 and H-8, a calmodulin antagonist W-7, and protein kinase C (PKC) activators, phorbol myristate acetate (PMA) and SC-9. H-7, more potent in inhibiting PKC than H-8, failed to attenuate the increase in permeability induced by TNF-alpha. Neither PMA nor SC-9 increased permeability. However, H-8, which is a potent inhibitor of cyclic nucleotide-dependent protein kinases, prevented the increase in permeability induced by TNF-alpha. These results suggest that protein kinase other than PKC are involved in the signal transduction in endothelial permeability increase induced by TNF-alpha. Calmodulin pathway may not be implicated in the increase in permeability induced by TNF-alpha.

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Citations

Mar 22, 2005·American Journal of Respiratory Cell and Molecular Biology·Sadatomo TasakaAkitoshi Ishizaka
Jul 12, 2005·American Journal of Physiology. Lung Cellular and Molecular Physiology·Makoto SawafujiKoichi Kobayashi
May 15, 2001·American Journal of Physiology. Lung Cellular and Molecular Physiology·I PetracheJ G Garcia

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