Inhibition of receptor loss during refrigeration increases the amount of terminal β-galactose on the platelet surface. (A-B) Flow cytometric analysis of terminal β-galactose on platelets treated with the p38 MAPK inhibitor SB203580 or the MP inhibitor GM6001 as detected with ECL FITC-labeled lectin. Lectin binding to fresh (RT) or refrigerated (48 hours) platelets in the absence or presence of 40μM SB203580 (A) or 100μM GM6001 (B) is shown. The ratio of mean fluorescence intensity binding to fresh platelets (RT) is plotted. Histograms report the mean ± SEM for 3 separate experiments. *P < .05, **P < .01, and ***P < .001. (C) Flow cytometric analysis of β-galactose exposure on glycoproteins detected with ECL FITC-labeled lectin. Lectin binding to fresh (RT) or longterm-refrigerated (48 hours) Adam17^+/+ and Adam17^ΔZn/ΔZn platelets is shown (n = 5); *P < .05 and **P < .01.