American Society of Hematology

Fig. 1.

$Fig. 1. The inhibition of ceramide-induced cell DNA fragmentation. Jurkat T cells were treated with 5 μmol/L of C2-ceramide (C2-C) in the absence or presence of various antagonists for 4 hours, washed with PBS, and fixed with ethanol. DNA content was determined by staining with 20 μg/mL PI and analyzed by FACScan (Becton Dickinson). Fraction of cells with sub-G1DNA content (M1 fraction in the diagram) were assessed with CELLFIT program (Becton Dickinson). CTR, untreated cell control. The inhibitors used were as follows: forskolin (F), 10 μmol/L; C60 D3 (D3), 100 μmol/L; PDTC, 200 μmol/L; Z-VAD-FK (ICEi), 300 μmol/L. The sub-G1 fractions were less than 6% for cells treated with inhibitors only. The exception was PDTC, in which a slightly elevated background death (8%) was observed.$

The inhibition of ceramide-induced cell DNA fragmentation. Jurkat T cells were treated with 5 μmol/L of C₂-ceramide (C2-C) in the absence or presence of various antagonists for 4 hours, washed with PBS, and fixed with ethanol. DNA content was determined by staining with 20 μg/mL PI and analyzed by FACScan (Becton Dickinson). Fraction of cells with sub-G₁DNA content (M1 fraction in the diagram) were assessed with CELLFIT program (Becton Dickinson). CTR, untreated cell control. The inhibitors used were as follows: forskolin (F), 10 μmol/L; C₆₀ D3 (D3), 100 μmol/L; PDTC, 200 μmol/L; Z-VAD-FK (ICEi), 300 μmol/L. The sub-G₁ fractions were less than 6% for cells treated with inhibitors only. The exception was PDTC, in which a slightly elevated background death (8%) was observed.

This Feature Is Available To Subscribers Only