ISSN:
1573-4919
Keywords:
pulmonary surfactant
;
lipopolysaccharide
;
TNFα
;
IL-1β
;
TypeII pneumocytes
;
phosphatidycholine secretion
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
Notes:
Abstract Tumor necrosis factor α and interleukin-1β increase surfactant secretion in type II pneumocytes in a time- and dose-dependent manner. This stimulatory effect was additive to that of lipopolysaccharide, suggesting that cytokines and lipopolysaccharide may exert their actions through different signal transduction pathways. Tumor necrosis factor α and interleukin-1β did not modify the increase on phosphatidylcholine secretion induced by the direct protein kinase C activator tetradecanoylphorbol 13-acetate, whereas this effect was inhibited by the protein kinase C inhibitors bisindolylmaleimide (2 × 10-6M) and 1-(5-isoquinolinylsulphonyl)-2-methyl piperazone (10-4M). In addition, the stimulatory effect of tumor necrosis factor α and interleukin-1β was not suppressed by the intracellular Ca2+ chelator BAPTA (5 × 10-6M) or by KN-62 (3 × 10-5M), a specific inhibitor of Ca2+-calmodulin-dependent protein kinase. These results suggest that tumor necrosis factor α or interleukin-1β stimulate phosphatidylcholine secretion via protein kinase C activation in a Ca2+ -independent manner.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1006997731607
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