AI Article Synopsis
- The study investigates how tumour necrosis factor-alpha (TNF-alpha) affects pulmonary endothelial permeability, relevant to adult respiratory distress syndrome.
- Various agents, including protein kinase inhibitors and activators, were tested, revealing that H-8 effectively reduced TNF-alpha-induced permeability increases, while H-7 did not.
- Findings suggest that pathways involving protein kinases other than PKC are crucial in TNF-alpha's influence on endothelial permeability, indicating calmodulin may not play a role in this process.
Article 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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| http://dx.doi.org/10.1111/j.1440-1843.1997.tb00055.x | DOI Listing |
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