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Studying the mechanisms that cause heart failure

  • Full or part time
    Dr Samuel Boateng
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

About This PhD Project

Project Description

Heart failure has a serious impact on our society and once diagnosed has a poor survival rate. In the United Kingdom, there are about 1.5 million people living with the after-effects of a heart attack, and this presents a huge economic burden each year. Worldwide, heart failure is becoming an increasing problem even in developing countries. There are many causes of heart failure which result in poor heart function. However, the exact mechanism by which heart failure occurs is still poorly understood. The goal of my laboratory is to determine how the heart and heart cells respond to the stresses that normally lead to heart failure. Understanding this process will lead to the production of new drugs which will help cure and prevent the disease. This project will involve cell/molecular biological techniques such as tissue culture, real-time RT-PCR, Western immunoblotting, gene over-expression and siRNA knockdown, confocal microscopy and much more.

If you choose to study in the Boateng lab you will experience an exciting and dynamic atmosphere with many opportunities to present your work at national and international conferences. The work in my lab has been extensively featured by the British Heart Foundation (the biggest supporter of cardiovascular research in the UK), the University of Reading and the BBC news. Please see the websites below for more details on our lab work.

http://www.bbc.co.uk/news/uk-england-berkshire-22443975

https://www.bhf.org.uk/heart-matters-magazine/research/sam-boateng

http://www.reading.ac.uk/internal/staffportal/news/articles/spsn-504278.aspx


Please contact me if you have any questions. I look forward to working with you.

References

Selected references

Paudyal A, Dewan S, Ikie C, Whalley BJ, de Tombe PP, Boateng SY. Nuclear accumulation of myocyte muscle LIM protein is regulated by heme oxygenase 1 and correlates with cardiac function in the transition to failure. J Physiol. 2016 Jun 15;594(12):3287-305.

Atkins JD, Boateng SY, Sorensen T, McGuffin LJ. Disorder Prediction Methods, Their Applicability to Different Protein Targets and Their Usefulness for Guiding Experimental Studies. Int J Mol Sci. 2015 Aug 13;16(8):19040-54.

Ravishankar D, Watson KA, Boateng SY, Green RJ, Greco F, Osborn HM. Exploring quercetin and luteolin derivatives as antiangiogenic agents. Eur J Med Chem. 2015 Jun 5;97:259-74.

Arif IS, Hooper CL, Greco F, Williams AC, Boateng SY. Increasing doxorubicin activity against breast cancer cells using PPARγ-ligands and by exploiting circadian rhythms. Br J Pharmacol. 2013 Apr 12. doi: 10.1111/bph.12202.

Hooper CL, Paudyal A, Dash PR and Boateng SY. Modulation of stretch-induced myocyte remodelling and gene expression by nitric oxide: A novel role for lipoma preferred partner in myofibrillogenesis. Am J Physiol Heart Circ Physiol. 2013 May;304(10):H1302-13. doi: 10.1152/ajpheart.00004.2013. Epub 2013 Mar 15

Hooper CL, Dash P and Boateng SY. Lipoma preferred partner is a mechanosensitive protein regulated by nitric oxide in the heart. FEBS Open Bio 2, 2012, Pages 135–144.

Boateng SY, Senyo SE, Qi L, Goldspink PH and Russell B. Myocyte remodelling in response to hypertrophic stimuli requires nucleocytoplasmic shuttling of muscle LIM protein. J Mol Cell Cardiol 47(4): 426-35 (2009).

-Associated editorial. MLP: A stress sensor goes nuclear. Editorial. J Mol Cell Cardiol 47(4): 423-425 (2009).

Boateng SY and Goldspink PH. Assembly and maintenance of the sarcomere night and day. Cardiovascular Research (Review). 2008;77(4):667-75 (2008).

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