UNIGE document Scientific Article
previous document  unige:7085  next document
add to browser collection
Title

Does protein kinase C control receptor-mediated phagocytosis in human neutrophils?

Authors
Andersson, T.
Fallman, M.
Stendahl, O.
Published in FEBS Letters. 1988, vol. 239, no. 2, p. 371-375
Abstract It was previously demonstrated that C3bi- but not IgG-mediated phagocytosis in human neutrophils is a Ca2+-independent process [(1985) Nature 315, 509-511]. The objective of this study was to elucidate the nature of an additional messenger signal(s) that may be involved in receptor-mediated phagocytosis in these cells. The C3bi- and IgG-mediated phagocytic ability of neutrophils was inhibited by forskolin, a potent activator of adenylate cyclase. It was found that forskolin induced a 3-fold increase in cAMP levels and simultaneously reduced the uptake of both C3bi- and IgG-opsonized particles by 65%. This inhibition was reversed by exposure to either phorbol myristate acetate (PMA) or diacylglycerol (OAG), which are both activators of protein kinase C, but not by the inactive analog 4 alpha-PMA. PMA could also restore the phagocytic ability of neutrophils with an experimentally impaired calcium response. These results suggest that activation of protein kinase C might be an important transducing signal controlling receptor-mediated phagocytosis in human neutrophils.
Keywords Cyclic AMP/bloodDiglycerides/pharmacologyHumansNeutrophils/drug effects/immunology/ physiologyPhagocytosisProtein Kinase C/ blood/physiologyReceptors, Immunologic/ physiologyTetradecanoylphorbol Acetate/pharmacology
Identifiers
PMID: 2846363
Full text
Article - document accessible for UNIGE members only Limited access to UNIGE
Structures
Citation
(ISO format)
ANDERSSON, T. et al. Does protein kinase C control receptor-mediated phagocytosis in human neutrophils?. In: FEBS Letters, 1988, vol. 239, n° 2, p. 371-375. https://archive-ouverte.unige.ch/unige:7085

183 hits

0 download

Update

Deposited on : 2010-06-21

Export document
Format :
Citation style :