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Hyperglycemia-induc...
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Saiepour, DanielUmeå universitet,Histologi med cellbiologi
(author)
Hyperglycemia-induced protein kinase C (PKC) activation inhibits phagocytosis of C3b- and IgG-opsonized yeast particles in normal human neutrophils
- Article/chapterEnglish2003
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LIBRIS-ID:oai:DiVA.org:umu-4928
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-4928URI
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https://doi.org/10.1155/EDR.2003.125DOI
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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The aim of this study was to investigate the effects of elevated glucose concentrations on complement receptor- and Fcgamma receptor-mediated phagocytosis in normal human neutrophils. D-Glucose at 15 or 25 mM dose-dependently inhibited both complement receptor- and Fcgamma receptor-mediated phagocytosis, as compared to that at a normal physiological glucose concentration. The protein kinase C (PKC) inhibitors GF109203X and Go6976 both dose-dependently and completely reversed the inhibitory effect of 25 mM D-glucose on phagocytosis. Complement receptor-mediated phagocytosis was dose-dependently inhibited by the cell permeable diacylglycerol analogue 1,2-dioctanoyl-sn-glycerol (DAG), an effect that was abolished by PKC inhibitors. Furthermore, suboptimal inhibitory concentrations of DAG and glucose showed an additive inhibitory effect on complement receptor-mediated phagocytosis. The authors conclude that elevated glucose concentrations can inhibit complement receptor and Fcgamma receptor-mediated phagocytosis in normal human neutrophils by activating PKCalpha and/or PKCbeta, an effect possibly mediated by DAG.
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Sehlin, JanoveUmeå universitet,Histologi med cellbiologi(Swepub:umu)jase0001
(author)
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Oldenborg, Per-ArneUmeå universitet,Histologi med cellbiologi(Swepub:umu)peol0001
(author)
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Umeå universitetHistologi med cellbiologi
(creator_code:org_t)
Related titles
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In:Experimental Diabesity Research4:2, s. 125-1321543-86001543-8619
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