Fig. 8 | Scientific Reports

Fig. 8

From: A design for an efficient functional panel that determines platelet exhaustion levels to differentiate responder and non-responder ITP patients

Fig. 8The alternative text for this image may have been generated using AI.

A comparison of the platelet functional panel in ITP patients, distinguishing between responders and non-responders, in relation to healthy individuals. (A) At baseline, platelets of healthy controls exhibit normal levels (N) of P-selectin expression, PAC-1 binding, and ROS generation. Following treatment with PMA, there is an increase in the levels of all three parameters in response. PMA has the ability to recruit and activate PKC. This enzyme induces platelet granule release, NOX activation, and the enhancement of inside-out signaling as well as RhoA and MAPK signaling pathways, leading to activation and clustering of integrin αIIbβ3. (B) In the platelets of “Responder” ITP, baseline levels of P-selectin expression, PAC-1 binding, and ROS generation were not significantly (NS) different from those in normal platelets. Following PMA treatment, all three factors showed an increase (slightly less than normal platelets). (C) In the platelets of “Non-Responder” ITP, the baseline levels of PAC-1 binding and ROS generation were not significantly (NS) different from those observed in normal platelets. Upon exposure to PMA, all three factors exhibited a decrease when compared to both normal platelets and the platelets of ITP responders. Fb, Fibrinogen; ITP, immune thrombocytopenia; MAPK, Mitogen-activated protein kinase; N, Normal; NS, Not Significant, NOX, NADPH oxidases; PKC, protein kinase C; PMA, Phorbol 12-Myristate 13-Acetate; ROS, Reactive Oxygen Species.

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