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. 2013 Jun 19;305(5):C519–C528. doi: 10.1152/ajpcell.00418.2012

Fig. 2.

Fig. 2.

PAK activation in platelets upon stimulation with thrombin. A: human platelets treated with vehicle (DMSO), the Rho kinase (ROCK) inhibitor Y-27632 (10 μM), or the Rac inhibitor EHT 1864 (50 μM) before stimulation with 1 U/ml thrombin (Thr). Platelet PAK activation was determined by Western blot for phosphorylation of PAK2-Ser192 and phosphorylation of the PAK substrate GIT1-Ser517 under basal (lane 1) and thrombin-stimulated conditions (lanes 2–4). B: human platelets treated with vehicle (0.1%, DMSO), the inhibitor of PAK activation IPA-3 (10 μM), or the inactive PAK inhibitor relative PIR 3.5 (10 μM) before stimulation with 1 U/ml thrombin (Thr). PAK activation determined by Western blot for PAK2-pSer20, PAK2-pSer192 and PAK2-pThr402 under basal (lane 1) and thrombin-stimulated conditions (lanes 2-4). C: resting and thrombin-stimulated platelets treated with vehicle (0.1% DMSO), IPA-3 (10 μM), or PIR 3.5 (10 μM) were fixed in paraformaldehyde and examined for filopodia formation by differential interference contrast (DIC) microscopy. Scale bar = 1 μm. D: distribution analysis of measured platelet filopodia lengths from resting and thrombin-stimulated platelets treated with vehicle, IPA-3, or PIR 3.5 (n = 600 per condition).