Microvesicles generated following traumatic brain injury induce platelet dysfunction via adenosine diphosphate...

Area of Science:

• Neuroscience
• Hematology
• Trauma Research

Background:

• Traumatic brain injury (TBI) can cause acute coagulopathy, characterized by platelet dysfunction and increased intracranial hemorrhage.
• Adenosine diphosphate (ADP)-induced platelet aggregation is reduced post-TBI.
• Circulating microvesicles (MVs) increase after TBI and are implicated in coagulopathy and platelet dysfunction.

Purpose of the Study:

• To investigate the role of post-TBI microvesicles (MVs) in platelet aggregation.
• To determine if MVs isolated from TBI mice affect platelet function in uninjured mice.

Main Methods:

• Moderate TBI was induced in mice using a weight-drop method.
• Whole blood, plasma, and MVs were isolated from TBI and sham mice.
• Platelet aggregation in response to ADP was measured using Multiplate impedance aggregometry.

Main Results:

• Post-TBI whole blood showed diminished ADP-induced platelet aggregation compared to sham.
• Post-TBI plasma and MVs reduced ADP-induced platelet aggregation in normal blood.
• MV-poor plasma from TBI mice did not affect aggregation in normal blood.

Conclusions:

• Acute TBI inhibits ADP-induced platelet aggregation in mice.
• Post-TBI MVs contribute to platelet dysfunction.
• Inhibition of the P2Y12 ADP receptor on MVs prevents platelet dysfunction.