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Hyperglycemia-induc...
Hyperglycemia-induced protein kinase C (PKC) activation inhibits phagocytosis of C3b- and IgG-opsonized yeast particles in normal human neutrophils
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- Saiepour, Daniel (författare)
- Umeå universitet,Histologi med cellbiologi
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- Sehlin, Janove (författare)
- Umeå universitet,Histologi med cellbiologi
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- Oldenborg, Per-Arne (författare)
- Umeå universitet,Histologi med cellbiologi
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(creator_code:org_t)
- 2003
- 2003
- Engelska.
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Ingår i: Experimental Diabesity Research. - 1543-8600 .- 1543-8619. ; 4:2, s. 125-132
- Relaterad länk:
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http://www.ncbi.nlm....
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
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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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- art (ämneskategori)
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