Dr Simon Bamforth
- Email: firstname.lastname@example.org
- Telephone: +44 (0) 191 241 8764
- Address: Institute of Genetic Medicine
International Centre for Life
Newcastle upon Tyne
1996 PhD, University College London
My PhD research investigated the structure and susceptibility of the blood-retinal barrier to immunological insult. This work was related to the clinical condition of uveitis, as well as being a model for the blood-brain barrier, which is vital for protecting the central nervous system from infection or blood borne molecules. My research demonstrated that a infiltration of leukocytes to the retina causes the blood-retinal barrier to breakdown, and it is the leukocytes themselves that cause this to occur.
1996-1998 Post-Doctoral Research Fellow
Max Planck Institute for Clinical and Physiological Research, Bad Nauheim, Germany
My first post-doctoral position extended my research on the blood-CNS barriers by focusing on the molecules that form the boundaries between cells – the tight junctions. Gaining knowledge as to how the cells control permeability across a selective interface, and how they prevent leakage from the blood to the neural parenchyma, was necessary to gain a fundamental understanding as to how this mechanism functions. This understanding could then be applied to preventing breakdown of these tight junctions during disease. My research focused on the role of a newly discovered tight junction molecule called occuldin. I demonstrated that a mutated form of this protein when over-expressed in epithelial cells, caused the tight junctions to fail.
1998 - 2008 Senior Post-Doctoral Research Fellow
Department of Cardiovascular Medicine, University of Oxford, UK
During my second post-doctoral position I developed a knockout mouse of the gene Cited2. This gene was predicted to play a vital role in development as it was linked to the function of the ubiquitously expressed transcriptional co-activators and histone acetyl transferases p300 and CBP, which are involved in heart and neural development. Cited2 was also shown to be upregulated in hypoxia, suggesting it may also play a role in disease. I generated the Cited2 knockout mouse and described its phenotype which comprised of complex cardiovascular, neural tube, adrenal and left-right patterning defects. I also contributed to the development and optimization of the MRI protocol to rapidly and non-destructively phenotype mouse fetuses by MRI.
2008 – 2013 British Heart Foundation Intermediate Basic Science Research Fellow
2014 – University Lecturer
Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, UK
My current research as an independent group leader is focusing on the roles of transcription factors during cardiovascular development as well as investigating the morphological process underlying heart and great vessel development. Combining these two elements of research will give us a deeper understanding of the molecular control of normal heart development as well as an understanding of the embryological etiology of congenital heart defects.
Genetics of cardiovascular development
Congenital cardiovascular malformations are among the most common birth defects, occurring in up to 1% of live births, and affect the outflow tract of the heart and the great vessels that arise from it. The aorta and pulmonary trunk emerge from the left and right ventricles respectively and connect to the pulmonary, carotid and subclavian arteries that supply blood to the lungs and the rest of the body. These blood vessels are derived from the pharyngeal arch arteries and develop during embryogenesis from a bilaterally symmetrical structure to a highly asymmetrical one through a complex remodelling process involving apoptosis and blood flow. When this developmental process fails, patients suffer from cardiovascular conditions such as Tetralogy of Fallot, common arterial trunk, transposition of the great arteries, interrupted aortic arch and anomalous right subclavian artery. In patients, some of these defects can be attributed to syndromes or chromosomal abnormalities (for example, DiGeorge Syndrome), but the majority occur through an unknown genetic component. My research group is investigating how certain genes, expressed within the developing pharyngeal arches, can control the correct development of the heart and its associated great vessels using transgenic models, imaging methodologies, gene expression patterns and next generation sequencing techniques. Gene mutations in transgenic models can be very informative in understanding how a gene controls certain developmental processes. We hope that our studies will result in mechanistic insight into how cardiovascular developmental disorders in humans may occur.
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**Post-Doctoral Research Associate position now available (6 month contract)**
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Module Leader and Lecturer: MRes Developmental Genetics (MMB8031)
Lecturer: Cardiovascular System Physiology (PSC2020)
Practical Leader: Practical Skills in Biomedical & Biomolecular Sciences 1 (CMB1005)
Seminar Leader: BSc Genetics (BGM1004)
- Bamforth SD, Anderson RH. Anomalous origin of the left pulmonary artery from the internal carotid artery. Cardiology in the Young 2016, 26(1), 143-144.
- Anderson RH, Bamforth SD, Spicer DE, Henderson DJ, Chaudhry B, Brown NA, Mohun TJ. Development and maldevelopment of the ventricular outflow tracts. In: Lacour-Gayet F; Bove EL; Hraška V; Morell V; Spray T, ed. Surgery of Conotruncal Anomalies. Cham, Switzerland: Springer International Publishing, 2016, pp.27-59.
- Bamforth SD, Anderson RH. Understanding the morphogenesis of the left-sided arterial duct in the setting of a right-sided aortic arch. Cardiology in the Young 2016, (ePub ahead of Print), 1-4.
- Suntratonpipat S, Bamforth SD, Johnson AL, Noga M, Anderson RH, Smallhorn J, Tham E. Childhood presentation of interrupted aortic arch with persistent carotid ducts. World Journal for Pediatric Congenital Heart Surgery 2015, 6(2), 335-338.
- Gupta SK, Bamforth SD, Anderson RH. How frequent is the fifth arch artery?. Cardiology in the Young 2015, 25(4), 628-646.
- Johnson A-L, Bamforth SD. Molecular pathways and animal models of truncus arteriosus. In: Congenital Heart Diseases: The Broken Heart: Clinical Features, Human Genetics and Molecular Pathways. Springer-Verlag Wien, 2015, pp.569-578.
- Hernandez LE, Shepard CW, Bamforth SD, Anderson RH. The Right Subclavian Artery Arising as the First Branch of a Left-Sided Aortic Arch. World Journal for Pediatric and Congenital Heart Surgery 2014, 5(3), 456-459.
- MacDonald ST, Bamforth SD, Bragança J, Chen C-M, Broadbent C, Schneider JE, Schwartz R, Bhattacharya S. A cell-autonomous role of Cited2 in controlling myocardial and coronary vascular development. European Heart Journal 2013, 34(32), 2557-2565.
- Bamforth SD, Chaudhry B, Bennett M, Wilson R, Mohun TJ, van Mierop LHS, Henderson DJ, Anderson RH. Clarification of the identity of the mammalian fifth pharyngeal arch artery. Clinical Anatomy 2013, 26(2), 173-182.
- Chen CM, Bentham J, Cosgrove C, Braganca J, Cuenda A, Bamforth SD, Schneider JE, Watkins H, Keavney B, Davies B, Bhattacharya S. Functional Significance of SRJ Domain Mutations in CITED2. PLoS One 2012, 7(10), e46256.
- Bamforth SD, Schneider JE, Bhattacharya S. High-throughput analysis of mouse embryos by magnetic resonance imaging. Cold Spring Harbor Protocols 2012, 2012(1), 93-101.
- Anderson RH, Chaudhry B, Mohun TJ, Bamforth SD, Hoyland D, Phillips HM, Webb S, Moorman AF, Brown NA, Henderson DJ. Normal and abnormal development of the intrapericardial arterial trunks in humans and mice. Cardiovascular Research 2012, 95(1), 108-115.
- Arthur HM, Bamforth SD. TGF beta Signaling and Congenital Heart Disease: Insights from Mouse Studies. Birth Defects Research Part A: Clinical and Molecular Teratology 2011, 91(6), 423-434.
- Michell A, Braganca J, Broadbent C, Joyce B, Franklyn A, Schneider JE, Bhattacharya S, Bamforth SD. A novel role for transcription factor Lmo4 in thymus development through genetic interaction with Cited2. Developmental Dynamics 2010, 239(7), 1988-1994.
- Bamforth SD, Venkatesh D, Broadbent C, Schneider JE, Bhattacharya S. THE ROLE OF AP-2 ALPHA IN THE DEVELOPMENT OF THE OUTFLOW TRACT AND PHARYNGEAL ARCH ARTERIES. In: HEART. 2009, BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND: B M J PUBLISHING GROUP.
- MacDonald ST, Bamforth SD, Chen CM, Farthing CR, Franklyn A, Broadbent C, Schneider JE, Saga Y, Lewandoski M, Bhattacharya S. Epiblastic Cited2 deficiency results in cardiac phenotypic heterogeneity and provides a mechanism for haploinsufficiency. Cardiovascular Research 2008, 79(3), 448-457.
- Bamforth SD, Braganca J, Farthing CR, Schneider JE, Broadbent C, Michell AC, Clarke K, Neubauer S, Norris D, Brown NA, Anderson RH, Bhattacharya S. Cited2 controls left-right patterning and heart development through a Nodal-Pitx2c pathway. Nature Genetics 2004, 36(11), 1189-1196.
- Schneider JE, Bose J, Bamforth SD, Gruber AD, Broadbent C, Clarke K, Neubauer S, Lengeling A, Bhattacharya S. Identification of cardiac malformations in mice lacking Ptdsr using a novel high-throughput magnetic resonance imaging technique. BMC Developmental Biology 2004, 4(1), 16.
- Schneider JE, Bamforth SD, Grieve SM, Clarke K, Bhattacharya S, Neubauer S. High-resolution, high-throughput magnetic paragraph sign resonance imaging of mouse embryonic paragraph sign anatomy using a fast gradient-echo sequence. Magnetic Resonance Materials in Physics, Biology and Medicine 2003, 16(1), 43-51.
- Schneider JE, Bamforth SD, Farthing CR, Clarke K, Neubauer S, Bhattacharya S. Rapid identification and 3D reconstruction of complex cardiac malformations in transgenic mouse embryos using fast gradient echo sequence magnetic resonance imaging. Journal of Molecular and Cellular Cardiology 2003, 35(2), 217-222.
- Bamforth SD, Braganca J, Eloranta JJ, Murdoch JN, Marques FIR, Kranc KR, Farza H, Henderson DJ, Hurst HC, Bhattacharya S. Cardiac malformations, adrenal agenesis, neural crest defects and exencephaly in mice lacking Cited2, a novel Tfap activator. Nature Genetics 2001, 29, 469-474.