2004
DOI: 10.4049/jimmunol.173.3.1596
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Antisense Knockdown of Sphingosine Kinase 1 in Human Macrophages Inhibits C5a Receptor-Dependent Signal Transduction, Ca2+ Signals, Enzyme Release, Cytokine Production, and Chemotaxis

Abstract: The anaphylatoxin C5a is produced following the activation of the complement system and is associated with a variety of pathologies, including septic shock and adult respiratory distress syndrome, and with immune complex-dependent diseases such as rheumatoid arthritis. C5a has been shown to regulate inflammatory functions by interacting with its receptor, C5aR, which belong to the rhodopsin family of seven-transmembrane GPCRs. However, the intracellular signaling pathways triggered by C5aR on immune-effector c… Show more

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Cited by 89 publications
(119 citation statements)
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“…In contradiction to other authors who described that SPHK2 is not detectable in monocytes or macrophages [14][15][16], we could demonstrate that monocytes indeed express SPHK2 although to a much lower degree than SPHK1 (Fig. 1).…”
Section: Discussioncontrasting
confidence: 99%
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“…In contradiction to other authors who described that SPHK2 is not detectable in monocytes or macrophages [14][15][16], we could demonstrate that monocytes indeed express SPHK2 although to a much lower degree than SPHK1 (Fig. 1).…”
Section: Discussioncontrasting
confidence: 99%
“…Our observation that inhibition of either Erk [3] or SphK (Fig. 3) each results in strongly reduced cytokine release from CXCL4-stimulated monocytes, extent corresponding findings for TNF-activated monocytes and C5a-treated macrophages [15,16]. Having in mind that in CXCL4-treated monocytes cytokine release as well as rescue from apoptosis are regulated by SphK1 as well as Erk the question arise whether these molecules might regulate each other.…”
Section: Discussionsupporting
confidence: 60%
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“…However, it was not clear from these studies whether interaction between CaM and hSK1 was required for the translocation or whether CaM was indirectly involved in the process. Also unclear was the potential involvement of CaM in the translocation of hSK1 to the plasma membrane observed to be induced by various other cellular stimuli, including platelet-derived growth factor (37), anaphylatoxin C5a (38), phorbol esters (13,39), and cross-linking of the Fc⑀RI immunoglobulin receptor (40). The identification of the CaM-binding site and generation of a CaM-binding deficient version of hSK1 in the current study enabled us to examine further the direct role of CaM in the cellular localization of hSK1.…”
Section: Mutagenesis Of Predicted Cam-binding Sites In Hsk1-hsk1 and mentioning
confidence: 99%