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. 2016 Oct 5;6(3):720–730. doi: 10.5966/sctm.2016-0104

Figure 5.

Figure 5

Direct inhibition of ADAM17 more effectively sustained GPIbα retention by cultured iPSC‐derived platelets than suppression of potential upstream activators of ADAM17. Percentages of the GPIbα+ population in CD41a+ iPSC‐derived platelets treated with the indicated inhibitors during the platelet production phase (days 21–23 or 24). KP‐457 (15 μmol/l), BIRB796 (10 μmol/l), MAPK/extracellular signal‐regulated kinase kinase inhibitor U0126 (10 μmol/l), IkB kinase β inhibitor BMS345541 (10 μmol/l), caspase inhibitor Z‐VAD (10 μmol/l) and protein kinase C inhibitor Ro31‐8220 (3 μmol/l) were used. Inhibition of potential ADAM17 activator molecules failed to prevent GPIbα shedding evoked by cultivation at 37°C. ∗, p < .05 versus vehicle group by Dunnett's test, n ≥ 3. Abbreviations: ADAM, a disintegrin and metalloproteinase; GP, glycoprotein; iPSC, induced pluripotent stem cell.