Figure 1
Figure 1. Stim1−/− neutrophils show defective SOCE in response to soluble agonists and thapsigargin. (A) WT neutrophils were labeled with Indo-1 AM and then stimulated with the indicated doses of fMLF (left panel) or MIP- 2 (right panel), and calcium flux was determined by flow cytometry. (B) WT and stim1−/− neutrophils were treated with 1 μM fMLP, 10 ng/mL MIP-2 (C), or 120 μg/mL bovine serum albumin/antibovine serum albumin immune complexes (IC) (D) in the absence (left panels) or presence (right panels) of 3 mM EGTA to chelate extracellular Ca2+. (E) WT and stim1−/− neutrophils were stimulated with thapsigargin (TG) (10 nM) in the presence (right panel) or absence (left panel) of 3 mM EGTA. Arrows indicate the addition of stimuli. Data are representative of at least 3 independent experiments.

Stim1/neutrophils show defective SOCE in response to soluble agonists and thapsigargin. (A) WT neutrophils were labeled with Indo-1 AM and then stimulated with the indicated doses of fMLF (left panel) or MIP- 2 (right panel), and calcium flux was determined by flow cytometry. (B) WT and stim1−/− neutrophils were treated with 1 μM fMLP, 10 ng/mL MIP-2 (C), or 120 μg/mL bovine serum albumin/antibovine serum albumin immune complexes (IC) (D) in the absence (left panels) or presence (right panels) of 3 mM EGTA to chelate extracellular Ca2+. (E) WT and stim1−/− neutrophils were stimulated with thapsigargin (TG) (10 nM) in the presence (right panel) or absence (left panel) of 3 mM EGTA. Arrows indicate the addition of stimuli. Data are representative of at least 3 independent experiments.

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