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Modulation of Ca²⁺ Signaling by Na⁺/Ca²⁺ Exchangers in Mast Cells

Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg, Germany

Mast cells rely on Ca²⁺ signaling to initiate activation programs leading to release of proinflammatory mediators. The interplay between Ca²⁺ release from internal stores and Ca²⁺ entry through store-operated Ca²⁺ channels has been extensively studied. Using rat basophilic leukemia (RBL) mast cells and murine bone marrow-derived mast cells, we examine the role of Na⁺/Ca²⁺ exchangers. Calcium imaging experiments and patch clamp current recordings revealed both K⁺-independent and K⁺-dependent components of Na⁺/Ca²⁺ exchange. Northern blot analysis indicated the predominant expression of the K⁺-dependent sodium-calcium exchanger NCKX3. Transcripts of the exchangers NCX3 and NCKX1 were additionally detected in RBL cells with RT-PCR. The Ca²⁺ clearance via Na⁺/Ca²⁺ exchange represented 50% of the total clearance when Ca²⁺ signals reached levels 200 nM. Ca²⁺ signaling and store-operated Ca²⁺ entry were strongly reduced by inverting the direction of Na⁺/Ca²⁺ exchange, indicating that Na⁺/Ca²⁺ exchangers normally extrude Ca²⁺ ions from cytosol and prevent the Ca²⁺-dependent inactivation of store-operated Ca²⁺ channels. Working in the Ca²⁺ efflux mode, Na⁺/Ca²⁺ exchangers such as NCKX3 and NCX3 might, therefore, play a role in the Ag-induced mast cell activation by controlling the sustained phase of Ca²⁺ mobilization.

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