COX-1(+/-)COX-2(-/-) genotype in mice is associated with shortened time to carotid artery occlusion through increased PAI-1.

ABSTRACT:

Background

We found a high incidence of thrombotic deaths in COX-1(+/-)COX-2(-/-) mice and sought to define the mechanism of these events. The cyclooxygenase products thromboxane A(2) and prostacyclin are important in the regulation of coagulation but their role in fibrinolysis is largely unexplored. PAI-1 blocks fibrinolysis by inhibiting plasminogen activator.

Aim

Our objective was to explain the mechanism of increased thrombosis associated with the COX-1(+/-)COX-2(-/-) genotype.

Methods

Carotid artery occlusion times were measured after photochemical injury. PAI-1 levels were measured in the plasma by ELISA. PAI-1 levels in the aorta were measured by RT-PCR and Western blotting. Urinary metabolites of Thromboxane A(2) and prostacyclin were measured by ELISA.

Res

SUBMITTER: Riehl TE 

PROVIDER: S-EPMC3687774 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature