Figure 3
Figure 3. UV-C activates αIIbβ3 and αIIbβ3-Δ724 in CHO cells. (A) CHO cells expressing αIIbβ3 show increased PAC-1 binding after UV-C irradiation. This binding is specific for αIIbβ3, as the antagonist tirofiban (1 μg/mL) inhibited PAC-1 binding in untreated cells and UV-C–irradiated cells. This graph is representative of 5 similar experiments. (B) CHO A5 cells (□) or CHO αIIbβ3-Δ724 cells (■) were irradiated with 1500 J/m2 UV-C. Activation of αIIbβ3 was measured with PAC-1 and was expressed as percentage of C17-FITC binding to correct for differences in αIIbβ3 expression. Binding of FITC-conjugated C17 to CHO/αIIbβ3 resulted in an MFI (FC17 − FIgG) value of 1165 (±165), and with CHO/αIIbβ3-Δ724 cells this value was 277 (± 91). Data represent the mean plus or minus SEM of 5 experiments.

UV-C activates αIIbβ3 and αIIbβ3-Δ724 in CHO cells. (A) CHO cells expressing αIIbβ3 show increased PAC-1 binding after UV-C irradiation. This binding is specific for αIIbβ3, as the antagonist tirofiban (1 μg/mL) inhibited PAC-1 binding in untreated cells and UV-C–irradiated cells. This graph is representative of 5 similar experiments. (B) CHO A5 cells (□) or CHO αIIbβ3-Δ724 cells (■) were irradiated with 1500 J/m2 UV-C. Activation of αIIbβ3 was measured with PAC-1 and was expressed as percentage of C17-FITC binding to correct for differences in αIIbβ3 expression. Binding of FITC-conjugated C17 to CHO/αIIbβ3 resulted in an MFI (FC17 − FIgG) value of 1165 (±165), and with CHO/αIIbβ3-Δ724 cells this value was 277 (± 91). Data represent the mean plus or minus SEM of 5 experiments.

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