Figure 2
Figure 2. αIIbβ3 activation by UV-C irradiation is not dependent on intracellular signaling. Platelets were preincubated for 30 minutes at 37°C with various inhibitors of platelet activation: 30 μM BAPTA/AM, 1 μM staurosporin (STSP), 10 μM Ly333531, or 20 μM forskolin and subsequently stimulated at 37°C for 5 minutes with 1 U/mL thrombin (□) or irradiated with 1500 J/m2 UV-C (■) as described in “Methods.” The PAC-1 binding to the controls (with DMSO added) was normalized to 100%, which had a mean fluorescence intensity (MFI; Fpac1 − F0) of 162 (±24) for the thrombin-stimulated platelets and an MFI of 44 (±10) for the UV-C–irradiated platelets. The mean fluorescence of PAC-1 to unstimulated platelets was used for background subtraction (F0). Data represent the mean plus or minus SD of 3 experiments.

αIIbβ3 activation by UV-C irradiation is not dependent on intracellular signaling. Platelets were preincubated for 30 minutes at 37°C with various inhibitors of platelet activation: 30 μM BAPTA/AM, 1 μM staurosporin (STSP), 10 μM Ly333531, or 20 μM forskolin and subsequently stimulated at 37°C for 5 minutes with 1 U/mL thrombin (□) or irradiated with 1500 J/m2 UV-C (■) as described in “Methods.” The PAC-1 binding to the controls (with DMSO added) was normalized to 100%, which had a mean fluorescence intensity (MFI; Fpac1 − F0) of 162 (±24) for the thrombin-stimulated platelets and an MFI of 44 (±10) for the UV-C–irradiated platelets. The mean fluorescence of PAC-1 to unstimulated platelets was used for background subtraction (F0). Data represent the mean plus or minus SD of 3 experiments.

Close Modal

or Create an Account

Close Modal
Close Modal