Understanding the role of the circadian molecular clock in the development of dilated cardiac myopathy and atrial fibrillation.
- Research Opportunity
- Honours students
- Number of Honour Places Available
- Number of Master Places Available
- Department / Centre
- Baker Department of Cardiometabolic Health
- Baker Heart and Diabetes Institute
|Associate Professor Morag Youngemail@example.com||385321111||Personal web page|
|Professor Julie McMullenfirstname.lastname@example.org||385321111||Personal web page|
Summary Virtually all cardiac functions, including the incidence of atrial fibrillation (AF) follow a circadian rhythm. Loss of appropriate timing keeping can lead to increased cardiovascular disease (CVD). Cardiac events often follow a circadian pattern, i.e. a heart attack or arrhythmia is more likely to occur in the morning. Atrial fibrillation (AF) or ‘arrhythmia’ in which your heart beats irregularly, reducing the heart’s ability to pump blood properly and increases the chance of a blood clots forming. This project will investigate whether the circadian molecular clock that underlies the circadian function of the heart, is dysregulated in a variety of cardiac disease models with and without AF. Models to be assessed include a transgenic mouse model with dilated cardiomyopathy (DCM) due to overexpression of mammalian sterile 20-like kinase 1 (Mst1), a model with DCM and AF due to overexpression of Mst1 together with reduced protective signalling due to reduced PI3K (Mst1-dnPI3K), and another transgenic model with DCM and AF due to overexpression of MURC (muscle-restricted coiled-coil; activates the RhoA/ROCK pathway). Techniques: RNA isolation, RT and PCR, Immunostaining, Histology, western block, immunostaining/histology, cell culture.
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Department / Centre
Baker Department of Cardiometabolic Health
Research NodeBaker Heart and Diabetes Institute
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