Why the study?
Does glycaemic control or Syk inhibition reduce GPVI-dependent platelet hyperreactivity in a rhesus monkey model of Type 1 diabetes?
Population
Nonhuman primate (rhesus monkey) model of Type 1 diabetes.
Comparison
Poorly controlled diabetes and in vitro… vs Well-controlled diabetes and healthy monkeys.
Design
Preclinical
Key result
Poorly controlled diabetes (~15 mM glucose) exacerbated GPVI-dependent platelet ROS generation and calcium flux, which was reversed to healthy levels by the Syk inhibitor BAY61-3606.
Authors
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May inform GPVI signaling in diabetic thrombosis; leaves open human translation and therapeutic implications.
Does glycaemic control or Syk inhibition reduce GPVI-dependent platelet hyperreactivity in a rhesus monkey model of Type 1 diabetes?
Poor glycaemic control exacerbates GPVI-dependent platelet hyperreactivity in a primate model of Type 1 diabetes, which can be mitigated by Syk inhibition, highlighting a potential novel antithrombotic target.
Arthur et al. (2013) studied Type 1 diabetes. Poorly controlled diabetes and Syk inhibitor BAY61-3606 vs. Well-controlled diabetes and healthy monkeys was evaluated on Platelet reactive oxygen species (ROS) generation, calcium mobilisation, receptor surface expression, and immature platelet fraction. Poorly controlled diabetes (~15 mM glucose) exacerbated GPVI-dependent platelet ROS generation and calcium flux, which was reversed to healthy levels by the Syk inhibitor BAY61-3606.