Fig. 5: Caspase activity and influence of caspase inhibition on radiation-induced cell death (24 h after IR) in unstimulated and stimulated PBLCs. | Cell Death & Disease

Fig. 5: Caspase activity and influence of caspase inhibition on radiation-induced cell death (24 h after IR) in unstimulated and stimulated PBLCs.

From: Sensitivity of CD3/CD28-stimulated versus non-stimulated lymphocytes to ionizing radiation and genotoxic anticancer drugs: key role of ATM in the differential radiation response

Fig. 5

a Stimulated PBLCs showed massive caspase-3/7 activity compared with unstimulated cells, which was independent from treatment with IR. Caspase activity was measured 24 h (Figure S8a for 6 h values) after treatment with IR (n = 3, mean value, SD, t-test *p < 0.05). b PARP-1 cleavage is a specific process induced by activated caspases. Cleavage of PARP-1 could only be determined in stimulated PBLCs (another representative western blot is shown in Figure S8b). c Treating PBLCs prior IR with a general caspase inhibitor (20 μM pan-caspase inhibitor Z-VAD-FMK) showed no influence on radiation-induced cell death in unstimulated and stimulated PBLCs. The graphs showed the radiation response without and with inhibitor treatment (n = 4, mean value, SD, t-test **p < 0.01, ***p < 0.001). The efficiency of the pan-caspase inhibitor was confirmed by a caspase activity assay (Figure S8c). d, e Inhibition of caspase-2 or caspase-1 showed no effect on radiation-induced cell death (n = 2–4, mean value, SD). f PBLCs were treated before and after irradiation with olaparib, a specific PARP inhibitor. There was no effect on radiation-induced cell death (n = 3, mean value, SEM, t-test *p < 0.05)

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