Abstract:

BACKGROUND: At present, the core control network, molecular etiology and mechanism of deep vein thrombosis is still not completely clear, furthermore, there is no ideal method for early diagnosis of deep venous thrombosis.
OBJECTIVE: To observe the prothrombotic role of Plaur and Plat in the vein endothelial cells in rats with traumatic deep vein thrombosis.
METHODS: Clamps plus lower limb immobilization with plaster spica were used to establish rat traumatic deep vein thrombosis models. Based on time points and whether thrombosis occurred, the experiment animals were divided into pre-thrombosis, thrombosis, and non-thrombosis groups, and then femoral vein endothelial cells were harvested at 2.5 and 25 hours after modeling.
RESULTS AND CONCLUSION: Gene chip analysis and real-time PCR results showed that after trauma 2.5 hours, mRNA expressions of Plaur, Plau and von Willebrand factor in the femoral vein were raised. In the process of thrombosis, Plaur, Plau and Von Willebrand factor mRNA expressions were significantly increased. Signal path analysis showed that the Plaur and Plau were upstream regulation genes for von Willebrand factor, and von Willebrand factor was the key gene for triggering platelet adhesion, aggregation and thrombosis. These findings imply that Plaur and Plau can be raised by up-regulation of von Willebrand factor expression, further to cause platelet adhesion and aggregation, and to promote traumatic deep vein thrombosis in rats.