Development of venous occlusions in mice transgenic for the plasminogen activator inhibitor-1 gene
Article Abstract:
Under normal conditions, there is a delicate balance between the factors that form blood clots and those which dissolve or prevent the formation of blood clots. If the balance is upset in one direction, thrombus formation can block blood vessels; if upset in the other direction, bleeding complications may result. One of the mechanisms of regulation is the availability and activity of plasminogen activators. Plasminogen activator can convert the zymogen plasminogen into the enzyme plasmin; the activated plasmin can then eat away at the fibrin strands making up a blood clot. (A zymogen is any protein which can be converted into an active enzyme). Plasminogen activators can be neutralized by plasminogen activator inhibitors, such as plasminogen activator inhibitor-1. Some researchers have suggested that too much plasminogen activator inhibitor may result in thrombotic disorders, and patients with some thrombotic disorders have been found to have excess plasminogen activator inhibitor in their blood. However, the cause- and-effect relationship is not certain. To determine if excess plasminogen-activator inhibitor-1 can cause the development of thrombosis, techniques of molecular biology were used to genetically engineer mice with elevated levels of inhibitor and a correspondingly low level of plasminogen activator activity. These mice were found to be susceptible to increased thrombus formation. Although occlusions were found in the veins, the arteries of these animals appeared normal. Similar venous clots are seen in human patients with protein C deficiency. The reason for the restriction of the thrombosis to the veins is not clear, but may involve changes in the endothelial lining which favor clot attachment. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1990
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Severe atherosclerosis in transgenic mice expressing simian cholesteryl ester transfer protein
Article Abstract:
Atherosclerosis is worse in transgenic mice expressing cholestrol ester transfer protein (CETP) than the non expressing controls-CETP-induced alterations in the lipoprotein profile, which causes the increase in lesion severity. The exchange of neutral lipids among the lipoproteins is mediated by CETP, a plasma protein.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1993
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A cholesteryl ester transfer protein inhibitor attenuates atherosclerosis in rabbits
Article Abstract:
Research is presented concerning the disulphide bond formed by cholesteryl ester transfer protein (CETP) and its inhibitors. One such inhibitor is found to inhibit the development of atherosclerosis in rabbits.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2000
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