IMPC: Analysis of the role of Cx57 in the regulation of platelet function, haemostasis and thrombosis
Lead Research Organisation:
University of Reading
Department Name: Clinical Health Sciences
Abstract
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Technical Summary
Platelets are small cells that control blood clotting. When they encounter cuts or damage to blood vessels they rapidly become sticky and stick to each other. This forms a plug, the first stage of clot formation that stops the bleeding as quickly as possible. Blood vessels become abnormal in cardiovascular disease and platelets can mistake these diseased vessels for cut vessels and consequently trigger the blood to form clots inside blood vessels (this is also known as thrombosis). This can clog up arteries and is the main trigger for heart attacks and strokes, which are frequently fatal. Scientists' successes in identifying how platelets sense healthy and damaged blood vessels, and also communicate with each other, has been critical in developing more effective drugs to prevent heart attacks and strokes, although such cardiovascular diseases still represent the principal causes of death in the UK. We are therefore focussing on increasing our understanding of the molecules and processes that enable platelets to be controlled in order to develop more effective medicines. We
have recently found a new protein called Cx57 on platelets and have produced considerable data to show that this is likely to contribute to thrombosis. In order to confirm this we need to study platelets that do not have this protein. In this project we will use mice that have been genetically engineered to lack Cx57. We will test what effect this has on platelet function, bleeding and thrombosis. This will form an important step to determine whether drugs that target this protein may be successful in preventing thrombosis and the other diseases in which platelets are involved.
have recently found a new protein called Cx57 on platelets and have produced considerable data to show that this is likely to contribute to thrombosis. In order to confirm this we need to study platelets that do not have this protein. In this project we will use mice that have been genetically engineered to lack Cx57. We will test what effect this has on platelet function, bleeding and thrombosis. This will form an important step to determine whether drugs that target this protein may be successful in preventing thrombosis and the other diseases in which platelets are involved.
Organisations
People |
ORCID iD |
Jonathan Gibbins (Principal Investigator) |
Publications
Description | Connexins as regulators of platelet function: Investigation of the mechanisms of action in the control of haemostasis and thrombosis |
Amount | £245,653 (GBP) |
Funding ID | PG/17/76/33082 |
Organisation | British Heart Foundation (BHF) |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 06/2018 |
End | 06/2022 |
Title | Generation of new transgenic mouse |
Description | We have generated a mouse in which he gene that encodes the transmembrane thiol isomerase TMX-1 is floxed. This will allow the gene to be deleted in a conditional manner through crossing with an appropriate Cre-expressing mouse line. Our initial work has involved the deletion of expression of this protein in platelets only. |
Type Of Material | Model of mechanisms or symptoms - mammalian in vivo |
Provided To Others? | No |
Impact | This will be made available once we have published our initial findings. |