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Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a
Author(s) -
Püschel Gerhard P.,
Hespeling Ursula,
Oppermann Martin,
Dieter Peter
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840180634
Subject(s) - prostanoid , anaphylatoxin , prostacyclin , glycogenolysis , prostaglandin , endocrinology , chemistry , medicine , prostaglandin e , zymosan , thromboxane , biology , biochemistry , platelet , complement system , immunology , in vitro , antibody , metabolism
Abstract Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a‐dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 μg/ml) dose‐dependently increased prostaglandin D 2 , thromboxane B 2 and prostaglandin F 2α formation in rat liver macrophages (Kupffer cells); (b) the C3amediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a‐elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C‐terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a‐dependent activation of hepatic glycogenolysis is mediated by way of a C3a‐induced prostanoid production in Kupffer cells. (HEPATOLOGY 1993;18:1516–1521.)

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