An inhibition of p38 mitogen activated protein kinase delays the platelet storage lesion

抑制 p38 丝裂原活化蛋白激酶可延缓血小板储存损伤

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作者:Andrey Skripchenko, Helen Awatefe, Dedeene Thompson-Montgomery, Andrew Myrup, Annette Turgeon, Stephen J Wagner

Conclusion

Signaling through p38 MAPK, but not ERK, is associated with platelet deterioration during storage.

Methods

A single Trima apheresis platelet unit (n = 12) was aliquoted into five CLX storage bags. Two aliquots were continuously agitated with or without MAPK inhibitors. Two aliquots were subjected to 48 hours of interruption of agitation with or without MAPK inhibitors. One aliquot contained the same amount of solvent vehicle used to deliver the inhibitor. Platelets were stored at 20-24°C for 7 days and sampled on Days 1, 4, and 7 for 18 in vitro parameters.

Results

Inhibition of p38 MAPK by VX-702 leads to better maintenance of all platelet in vitro storage parameters including platelet mitochondrial function. Accelerated by interruption of agitation, the platelet storage lesion of units stored with VX-702 was diminished to that of platelets stored with continuous agitation. Inhibition of ERK MAPK did not ameliorate decrements in any in vitro platelet properties.

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