{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Riehl TE"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS"],"pagination":["350-60"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3687774"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(2)"],"pubmed_abstract":["<h4>Background</h4>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.<h4>Aim</h4>Our objective was to explain the mechanism of increased thrombosis associated with the COX-1(+/-)COX-2(-/-) genotype.<h4>Methods</h4>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.<h4>Res"],"journal":["Journal of thrombosis and haemostasis : JTH"],"pubmed_title":["COX-1(+/-)COX-2(-/-) genotype in mice is associated with shortened time to carotid artery occlusion through increased PAI-1."],"pmcid":["PMC3687774"],"funding_grant_id":["DK33165","R01 DK033165-22","R01 DK033165","R01 DK055753-13","DK55753","HL55520","R01 HL055520","R01 DK055753","R37 DK033165"],"pubmed_authors":["Stenson WF","Tollefsen DM","Zheng L","Greco S","He L","Riehl TE"],"additional_accession":[]},"is_claimable":false,"name":"COX-1(+/-)COX-2(-/-) genotype in mice is associated with shortened time to carotid artery occlusion through increased PAI-1.","description":"<h4>Background</h4>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.<h4>Aim</h4>Our objective was to explain the mechanism of increased thrombosis associated with the COX-1(+/-)COX-2(-/-) genotype.<h4>Methods</h4>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.<h4>Res","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Feb","modification":"2025-04-07T12:58:44.54Z","creation":"2019-03-27T01:11:54Z"},"accession":"S-EPMC3687774","cross_references":{"pubmed":["21138526"],"doi":["10.1111/j.1538-7836.2010.04156.x"]}}