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. 2018 Jul 10;9:875. doi: 10.3389/fphys.2018.00875

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Copyright © 2018 Russo, Femminò, Barale, Tullio, Geuna, Cavalot, Pagliaro and Penna.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Infarct size expressed as percent of area at risk (A,B), and platelet ROS-infarct size correlations (C,D). (A) Washed platelets derived from healthy subjects (h-PLT) limited infarct size. The infarct size in hearts treated with platelets derived from diabetic patients (d-PLT) was higher than that observed in hearts pretreated with h-PLT. (B) The infarct size limitation effects of h-PLTs was abrogated by the blocker of S1P receptors, VPC23019, the antagonist of ERK1/2, U0126, the inhibitor of PI3K, LY or the antagonist of PKC, CHE. ^∗p < 0.005 vs. h-PLT; ^#p < 0.005 vs. I/R; NS, not significant (Newman–Keuls multiple-range test). (C) Correlation between ROS platelet levels and infarct size for the d-PLT group (n = 7; linear regression). (D) correlation between ROS platelet levels and infarct size for the h-PLT group (n = 7; linear regression).