Staff Profile:Dr Sam Boateng

Name::
Position / Job Title:
RCUK Research Fellow
Responsibilities:
Areas of Interest:
Heart failure has a serious impact on our society and once diagnosed has a 5 year survival rate worse than most cancers, with 40% of patients dying within a year. In the United Kingdom about 63,000 new cases are diagnosed each year with an economic burden of over £500 million. Heart failure may occur as a result of a heart attack or prolonged high blood pressure. In contrast, exercise leads to beneficial myocardial adaptation. The pathways that lead to either beneficial physiological or detrimental pathological adaptation are still poorly understood. The primary goal of my laboratory is to determine the mechanisms of myocardial adaptation and cardiac hypertrophy in response to mechanical stress.

Circadian proteins in the heart

Humans are well adapted to the cycle of night and day which regulates our sleep/wake pattern. The organs in our bodies are also adapted to anticipate the changes in physical activity that accompany this diurnal cycle (the cycle of night and day). At the cellular level, it is thought that up to 30% of the transcriptome is circadianly regulated. These genes are under the influence of specific circadian proteins which respond directly to the diurnal cycle. Recently, a number of studies have shown that many circadian genes are abnormally expressed and regulated in heart failure. Circadian genes in the heart allow the organ to anticipate the changes in demand that occur over a 24 hour period. Impaired circadian function may therefore prevent the heart from adjusting adequately to the diurnal variation in energy demand, leading to increased myocardial stress. My laboratory is trying to determine the function of these circadian proteins in the cardiac myocyte and whether abnormal function of these genes is implicated in human heart failure.

Mechanosensing in the heart

Cells within the myocardium are constantly remodelling through a process of mRNA translation and protein turnover. This homeostasis requires molecular sensors that constantly assess the cell environment. There is growing evidence that a number of cytoplasmic, plasma membrane and cytoskeletal proteins cycle constantly through the nucleus. These cycling proteins are thought to act as messengers and transcription factors, allowing the nuclear machinery to respond quickly to local changes. In myocytes, the Z-disk within the myofilaments harbours some of these nucleocytoplasmic shuttling proteins that are thought to be involved in mehanosensing (the sensing of mechanical forces and their translation into a biological response). The mechanosensing machinery allows myocytes to adapt to mechanical stimuli. A loss of mechanosensing is hypothesized to contribute to the transition from an adaptive to a maladaptive hypertrophy, leading to heart failure. My laboratory is trying to understand the function of these mechanosensing proteins in cardiac myocytes and their role in the failing human heart.

I am also a Adjunct Research Assistant Professor at the University of Illinois at Chicago, Department of Physiology and Biophysics.

Research groups / Centres:
Publications:
  •  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).
  • 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).
  • Boateng SY, Berlin JB, Geenen DL, Margulies KB, de Tombe PP and Russell B. Cardiac dysfunction and heart failure are associated with abnormalities in the subcellular distribution and amounts of oligomeric muscle LIM protein. Am J Physiol-Heart Circ Physiol 292(1):H259-69 (2007).
  • Lixin Qi and Boateng SY. The circadian protein Clock localizes to the sarcomeric Z-disk and is a sensor of myofilament cross-bridge activity in cardiac myocytes. Biochem Biophys Res Comm 352(4):1054-1059 (2006).
  • Lateef S, Boateng SY, Ahluwalia N, Hartman TJ, Hanley L and Russell B. Three-dimensional chemical structures by protein functionalised micron sized beads bound to polylysine coated silicone surfaces. J Biomed Mater Res A: 72A(4):373-80 (2005).
  • Boateng SY, Lateef S, Hartman TJ, Hanley L and Russell B. RGD and YIGSR synthetic peptides facilitate identical cellular adhesion as laminin and fibronectin but alter the physiology of neonatal cardiac myocytes. Am J Physiol Cell Physiol. (2005) Jan;288(1):C30-8. Epub 2004 Sep 15.
  • Boateng SY, Hartman TJ, Ahluwalia N, Vidula H, Desai TA and Russell B. Inhibition of fibroblast proliferation using silicone micropegs: Implications for cardiac tissue engineering and cell culturing. Am J Physiol-Cell Physiology 285:C171-C182 (2003).
  • Boateng S, Lateef SS, Crot CA, Motlagh D, Desai T, Samarel AM, Russell B and Hanley L. Peptides bound to silicone membranes and 3D micro fabrication for cardiac cell culture. Advanced Materials 14(6):461-463 (2002).
  • Lateef SS, Boateng S, Hartman TJ, Crot CA, Russell B and Hanley L. GRGDSP peptide bound silicone membranes withstand mechanical flexing in vitro and display enhanced fibroblast adhesion. Biomaterials 23:3159-3168 (2002).
  • Boateng SY, Naqvi R, Macleod K, Yacoub M and Boheler K. Short term low dose ramipril treatment normalises myocyte relaxation and calcium handling following cardiac hypertrophy in rats. Am J Physiol-Heart Circ Physiol 280(3):H1029-38 (2001).
  • Lateef S, Boateng S, Hartman T, Crot C, Russell B and Hanley L. Stretching and fibroblast growth on GRGDSP-peptide modified silicone membranes (Review). Polymeric materials: Science and Engineering 85:403-404 (2001).
  • Nikcevic G, Perhonen M, Boateng S and Russell B. Translation is regulated via the 3' untranslated region of a-myosin heavy chain mRNA by calcium, but not by its localization. J Muscle Res Cell Motil. 21(6):599-607 (2000).
  • Ribadeau-Dumas A, Brady M, Boateng SY, Schwartz K and Boheler KR. Sarco(Endo)plasmic reticulum Ca2+-ATPase (SERCA2) gene products are regulated post-transcriptionally during rat cardiac development. Cardiovas Res 43: 426-436 (1999).
  • Ationu A and Boateng S. The role of natriuretic peptides in cardiovascular disorders and human cardiac allografts (Review). Int J Mol Med 2: 235-239 (1998).
  • Boateng SY, Seymour A-M, Bhutta N, Dunn M, Yacoub M and Boheler K. Sub-antihypertensive doses of ramipril normalises calcium ATPase expression and function following cardiac hypertrophy in rats. J Mol Cell Cardiol. 30(12):2683-94 (1998).
  • Boateng S, Seymour A-M, Dunn M, Yacoub M and Boheler K. Inhibition of endogenous cardiac phosphatase activity and measurement of sarcoplasmic reticulum calcium uptake: a possible role of phospholamban phosphorylation in the hypertrophied myocardium. Biochem Biophys Res Comm 239: 701-705 (1997).
  • MU Koban, SY Boateng and K Boheler, The role of the sarcoplasmic reticulum calcium ATPase and its regulatory protein phospholamban in the developing myocardium. In: The Developing Heart (B.Ostadal: M. Nagano: N. Takeda: N.S Dhalla, eds) Lippincott-Ravens Publishers, New York, (1997).
  • Amarni M, Corbett J, Boateng SY, Dunn MJ and Yacoub MH. Kinetics of induction and protective effect of heat shock proteins following cardioplegic arrest. Ann-Thorac-Surg 61(5): 1407-11 (1996).
  • Amarni M, Corbett J, Allen NJ, O.Shea J, Boateng SY, May AJ, Dunn MJ and Yacoub MH. Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest. Ann-Thorac-Surg 57(1):157-160 (1994).

Current funding:

Royal Society grant
Principle investigator: Samuel Boateng
Award total £14,913 (1/9/2008 - 31/8/2009)
Project title: Mechanical stimulation of heart cells as a model of heart failure in vitro.

Research Endowment Trust Fund Studentship
University of Reading
£51,000 for 3 years (1/10/2008 - 30/9/2011)
Focal adhesion proteins and cardiac fibroblast function.

Marie Curie International Reintegration grant
European Commission (Framework Seven Programme)
Reference number: H5037400 (1/1/2008 - 31/12/2011)
Principle investigator: Samuel Boateng
EUR 25,000 per year for 4 years (award total EUR 100,000)
Nucleo-cytoplasmic shuttling proteins and mechano-signalling in cardiac myocytes.

Scientist Development grant
American Heart Association
Reference number: 0630307N (1/1/2006-31/12/2009)
Principle investigator: Samuel Boateng
$65,000 per year for 4 years ($260,000 total award)
The role of rest periods in myocyte adaptation to mechanical stimulation.

Contact Details

Email:
s.boateng@reading.ac.uk
Telephone:

+44 (0)118 378 7041

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