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dc.contributor.authorVenge, Per
dc.contributor.authorMoberg, Lena
dc.contributor.authorBjörnsson, Eythor
dc.contributor.authorBergström, Mats
dc.contributor.authorLångström, Bengt
dc.contributor.authorHåkansson, Lena
dc.date.accessioned2006-09-21T10:58:21Z
dc.date.available2006-09-21T10:58:21Z
dc.date.issued2003-10-01
dc.identifier.citationRespir Med 2003, 97(10):1109-19en
dc.identifier.issn0954-6111
dc.identifier.pmid14561018
dc.identifier.doidoi:10.1016/S0954-6111(03)00142-2
dc.identifier.otherPAD12
dc.identifier.urihttp://hdl.handle.net/2336/4541
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Link fielden
dc.description.abstractA link between glucose transport and apoptosis was suggested. We studied the mechanisms of glucose transport in human eosinophils by means of the uptake of the positron emitting analogue, 18Fluoro-2-Deoxyglucose (FDG) and apoptosis by means of flow cytometry. FDG uptake was inhibited by antibodies to GLUT1, 3 and 4 and by cytochalasin B. The anti-apoptotic principles IL-5, GM-CSF, IL-3 enhanced the uptake, whereas the apoptosis-inducing principles anti-CD95 (anti-Fas) and exposure to serum-coated Sephadex particles caused a reduction. Also TNF-alpha enhanced the uptake. Other cytokines such as IL-2, IL-4, IL-8, RANTES and MCP-3 had no effect on the glucose uptake. 2-Deoxyglucose, antibodies to GLUT4 and CD95 induced apoptosis. The basal FDG-uptake was unaffected by PKC inhibitors Ro-31-8220, Gö-6983 and Gö-6976, whereas the latter inhibited the IL-5-enhanced uptake possibly due to the inhibition of PKC(mu). Protein tyrosine kinase and PI-3 kinase inhibitors inhibited IL-5-enhanced FDG-uptake only. In contrast MEK inhibitors inhibited the basal uptake only. Inhibitors of p38 MAPkinase inhibited both basal and IL-5 enhanced uptake. We conclude that glucose uptake in eosinophils is governed by specific intracellular mechanisms involving mobilization of GLUTs, Ca2+ and the activation of the MAP kinase pathway and that the IL-5-enhanced uptake uniquely seems to involve PKC(mu) activity. Our results suggest a close link between apoptosis and glucose transport in human eosinophils.
dc.language.isoenen
dc.publisherW.B. Saundersen
dc.relation.urlhttp://www.sciencedirect.com/science/article/B6WWS-48B094H-4/2/1faafa3fda9e15554409888cedeebbecen
dc.subject.meshApoptosisen
dc.subject.meshBasal Metabolismeb
dc.subject.meshBiological Transporten
dc.subject.meshCells, Cultureden
dc.subject.meshCytokinesen
dc.subject.meshEosinophilsen
dc.subject.meshFlow Cytometryen
dc.subject.meshFluorodeoxyglucose F18en
dc.subject.meshGlucoseen
dc.subject.meshHumansen
dc.subject.meshRadiopharmaceuticalsen
dc.subject.meshResearch Support, Non-U.S. Gov'ten
dc.subject.meshSignal Transductionen
dc.titleMechanisms of basal and cytokine-induced uptake of glucose in normal human eosinophils: relation to apoptosisen
dc.typeArticleen
dc.identifier.journalRespiratory medicineen
dc.format.digYES
html.description.abstractA link between glucose transport and apoptosis was suggested. We studied the mechanisms of glucose transport in human eosinophils by means of the uptake of the positron emitting analogue, 18Fluoro-2-Deoxyglucose (FDG) and apoptosis by means of flow cytometry. FDG uptake was inhibited by antibodies to GLUT1, 3 and 4 and by cytochalasin B. The anti-apoptotic principles IL-5, GM-CSF, IL-3 enhanced the uptake, whereas the apoptosis-inducing principles anti-CD95 (anti-Fas) and exposure to serum-coated Sephadex particles caused a reduction. Also TNF-alpha enhanced the uptake. Other cytokines such as IL-2, IL-4, IL-8, RANTES and MCP-3 had no effect on the glucose uptake. 2-Deoxyglucose, antibodies to GLUT4 and CD95 induced apoptosis. The basal FDG-uptake was unaffected by PKC inhibitors Ro-31-8220, Gö-6983 and Gö-6976, whereas the latter inhibited the IL-5-enhanced uptake possibly due to the inhibition of PKC(mu). Protein tyrosine kinase and PI-3 kinase inhibitors inhibited IL-5-enhanced FDG-uptake only. In contrast MEK inhibitors inhibited the basal uptake only. Inhibitors of p38 MAPkinase inhibited both basal and IL-5 enhanced uptake. We conclude that glucose uptake in eosinophils is governed by specific intracellular mechanisms involving mobilization of GLUTs, Ca2+ and the activation of the MAP kinase pathway and that the IL-5-enhanced uptake uniquely seems to involve PKC(mu) activity. Our results suggest a close link between apoptosis and glucose transport in human eosinophils.


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