Cross-linking of FcɛRI causes Ca2+ mobilization via a sphingosine kinase pathway in a clathrin-dependent manner

Ryu, Seung Duk; Lee, Hyun Sil; Suk, Ho Young; Park, Chang Shin; Choi, Oksoon Hong

doi:10.1016/j.ceca.2008.07.002

Cited by 17 publications

(13 citation statements)

References 66 publications

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“…FccRI stimulation of U937 macrophages by cross-linking antibodies mobilized calcium from intracellular stores by activating sphingosine kinase [36]. Moreover, in mast cells, activation of FceRI generated Ca 2+ -signals that depended on sphingosine-1-phosphate production [37,38]. A contradictory report also exists, as FccRII-mediated calcium signalling in neutrophils allegedly was not inhibited by the sphingosine kinase inhibitor DMS [39].…”

Section: Discussionmentioning

confidence: 94%

C‐Reactive Protein Triggers Calcium Signalling in Human Neutrophilic Granulocytes via FcγRIIa in an Allele‐Specific Way

et al. 2013

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C-reactive protein (CRP) binds to Fcc-receptors, FccRIIa (CD32) with high affinity and to FccRIa (CD64) with low affinity. The binding to CD32 has been shown to be allele specific, that is, it binds to R/R131 but not to H/H131. Little is known about the cooperation of CRP and neutrophilic granulocytes (PMNs) in inflammatory reactions. The purpose of the present study was to examine CRP signalling in human PMNs, and whether this signalling is also allele specific. Cytosolic calcium of PMN was measured in a single-cell digital imaging system. Receptor expression and polymorphism were studied by real-time RT-PCR, flow cytometry and standard PCR. C-reactive protein induced cytosolic calcium signals in PMNs from homozygote R/R131donors, but not in PMNs from heterozygote R/H131 donors. However, after the heterozygote PMNs had been incubated with IFN-c (100 U/ml) for 2 h, both the proportion of cells responding and the size of the CRP-induced calcium signals increased. IFN-c increased mRNA expression of CD64 about fivefold and surface protein expression of CD64 about fourfold. The calcium signal elicited by CRP was augmented by PMN adhesion to fibronectin, but almost totally abrogated by sphingosine kinase inhibitors. The signals were partly dependent on calcium influx. In conclusion, calcium signalling instigated by CRP in human PMN is FccRIIa allele specific, as R/R131 responded to CRP, whereas R/H131 did not. However, increased expression of FccRIa (CD64), stimulated by IFN-c, can augment calcium signalling by CRP in low-responders. This suggests that the state of the PMNs, as well as the genetic origin, affect sensitivity for CRP.

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Section: Discussionmentioning

confidence: 94%

C‐Reactive Protein Triggers Calcium Signalling in Human Neutrophilic Granulocytes via FcγRIIa in an Allele‐Specific Way

et al. 2013

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“…Calcium is needed for degranulation and SphKs have been linked to calcium responses in IgE/Ag-activated MC (21, 24, 26, 47). Consistent with the effect on degranulation, calcium responses were reduced in both PDMC and BMMC (Fig.…”

Section: Resultsmentioning

confidence: 99%

Usage of Sphingosine Kinase Isoforms in Mast Cells Is Species and/or Cell Type Determined

Dillahunt

Sargent

Suzuki

et al. 2013

The Journal of Immunology

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FcεRI engagement in mast cells (MC) induces the activation of two distinct sphingosine kinase isoforms (SphK1 and SphK2) to produce sphingosine-1-phosphate, a mediator essential for MC responses. While embryonic derived SphK2-null MC showed impaired responses to antigen, RNA silencing studies on other MC types indicated a dominant role for SphK1. Given the known functional heterogeneity of MC, we explored whether the reported differences in SphK1 or SphK2 usage could be reflective of phenotypic differences between MC populations. Using lentiviral-based short hairpin RNA to silence SphK1 or SphK2 we found that SphK2 is required for murine MC degranulation, calcium mobilization, cytokine and leukotriene production irrespective of the tissue from which the MC progenitors were derived, the stage of MC granule maturity, or the conditions used for differentiation. This was consistent with the lack of a full allergic response in SphK2 -null mice challenged to undergo passive cutaneous anaphylaxis. A redundant role for both SphKs was uncovered, however, in chemotaxis towards antigen in all MC types tested and in TNF-α production in certain MC types. In contrast, human MC (HuMC) responses were dependent only on SphK1, associating with a more robust expression of this isoform and a more varied representation of SphK variants relative to murine MC. The findings show that the function of SphK1 and SphK2 can be interchangeable in MC; however, an important determinant of SphK isoform usage is the species of origin and an influencing factor, the tissue from which MC may be derived and/or their differentiation state.

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“…This calcium mobilization was recently demonstrated to be dependent on clathrin [47]. It has also been suggested that both InsP 3 and S1P contribute to FcεRI-induced calcium release from the endoplasmic reticulum and that production of InsP 3 is necessary for S1P to cause calcium mobilization from the endoplasmic reticulum [48].…”

Section: Intracellular Actions Of S1p In Mast Cellsmentioning

confidence: 95%

Sphingosine-1-phosphate synthesis and functions in mast cells

Price

Oskeritzian²,

Milstien³

et al. 2008

Future Lipidology

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Sphingolipids are not only major lipid components of all eukaryotic cell membranes, but they also comprise an important family of bioactive signaling molecules that regulate a diverse array of biological responses. The sphingolipid metabolite sphingosine-1-phosphate (S1P), is a key regulator of immune responses. Cellular levels of S1P are determined by the balance between its synthesis, involving two sphingosine kinases (SphK1 and SphK2), and its degradation, involving S1P lyase and S1P phosphatases. S1P mainly signals through its cell-surface receptors and may also have intracellular functions. S1P has important functions in mast cells – the major effectors of allergic responses. Antigen triggering of IgE receptors on mast cells activates both SphKs resulting in the production of S1P that is released and regulates and amplifies mast cell functions, including degranulation as well as cytokine and chemokine release.

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Cross-linking of FcɛRI causes Ca2+ mobilization via a sphingosine kinase pathway in a clathrin-dependent manner

Cited by 17 publications

References 66 publications

C‐Reactive Protein Triggers Calcium Signalling in Human Neutrophilic Granulocytes via FcγRIIa in an Allele‐Specific Way

C‐Reactive Protein Triggers Calcium Signalling in Human Neutrophilic Granulocytes via FcγRIIa in an Allele‐Specific Way

Usage of Sphingosine Kinase Isoforms in Mast Cells Is Species and/or Cell Type Determined

Sphingosine-1-phosphate synthesis and functions in mast cells

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