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Staff Profile

Dr Simon Bamforth

Senior Lecturer

Background

I am a member of the Biosciences Institute and Deputy Lead for the Reproduction Development and Child Health research theme. I am also affiliated with the Vascular Biology and Medicine research theme.

Career to date:

2022 - Senior Lecturer

2014 – 2022         Lecturer

Biosciences Institute, Newcastle University, UK

My current research 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. We are currently using single cell RNA-sequencing of embryonic tissue to unravel the complex genetic regulatory networks that control arch artery development.

Areas of expertise

  • Genetics of cardiovascular development
  • Cardiovascular anatomy

Google scholar: Click here.

SCOPUS: Click here.

2008 – 2013 British Heart Foundation Intermediate Basic Science Research Fellow

Biosciences Institute, Newcastle University, UK

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.  

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 occludin. I demonstrated that a mutated form of this protein when over-expressed in epithelial cells, caused the tight junctions to fail.

1996              PhD, University College London

Institute of Ophthalmology, London, UK

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 an infiltration of leukocytes to the retina causes the blood-retinal barrier to break down, and it is the leukocytes themselves that cause this to occur.



 

 

 

Research

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.

Click here for more details about my research.




Teaching

Deputy Degree Programme Director and Lead for MRes Projects (MMB8098)


Lecturer: Genetics of Human Development (MMB8031) (Former Module Lead, 2017-2024)

Lecturer: Cardiovascular System Physiology (PSC2020)

Lecturer: Medical Genomics: from DNA to disease (BGM2057)

Practical Leader: Practical Skills in Biomedical & Biomolecular Sciences 1 (CMB1005)

Seminar Leader: Genetics (BGM1004)



 

Publications