Dr Raewyn Carol Poulsen

Biography

Dr Poulsen returned to New Zealand in late 2013 after nearly 6 years of post-doctoral training at the Botnar Research Centre, Institute of Musculoskeletal Sciences, University of Oxford, UK. She is a cell biologist with expertise in cell signalling. Dr Poulsen currently holds a Sir Charles Hercus Health Research Fellowship (Health Research Council of New Zealand). 

Research | Current

Our research involves the study of cell signalling pathways to understand disease pathogenesis and to identify novel drug targets for treatment. A major focus of our work is osteoarthritis. Osteoarthritis is the leading cause of disability in adults worldwide. Despite its prevalence, there are no disease-modifying therapies available to treat osteoarthritis or slow the progression of disease. Our work has uncovered novel mechanisms involved in osteoarthritis development and we are currently investigating new pharmaceutical strategies to target these mechanisms. Recently, we identified that changes to the chondrocyte circadian clock, a key regulator of cell behaviour and cell differentiation, occur in human osteoarthritis and that these changes contribute to disease development. Current research projects in our group include:

Peripheral circadian clock disruption as a mechanism for disease

Most, if not all, cells in the body contain a circadian clock. Cell clocks are responsible for regulating the timing of cellular activities. They help ensure that opposing activities occur at different times and that mutually dependent processes occur concurrently. Circadian clock disruption is linked with a number of diseases including cancer and diabetes. In 2016, we demonstarted that the chondrocyte clock is altered in osteoarthritis. Since then, a number of studies have shown that chondrocyte clock disruption may contribute to osteoarthritis development. We are interested in determining how cell clocks are regulated, how clocks in neighbouring cells within a tissue are synchronised and why clocks are disrupted in disease. We are currently investigating how the clock controls chondrocyte behaviour and the causes of clock disruption in osteoarthritis. With collaborators in the School of Medical Sciences, we are also investigating the role of peripheral circadian clock disruption in cancer.

 

Bone-cartilage cross-talk in the development of osteoarthritis

Although loss of joint cartilage is a characteristic feature of osteoarthritis, there is evidence that disease actually initiates in bone. We are investigating how cells within different tissues communicate with each other. At present we are studying the impact of signals from bone cells, particularly osteocytes, in controlling the behaviour of chondrocytes. Aberrant signals from osteocytes may cause chondrocytes to alter their behaviour, contributing to the development of osteoarthritis.

 

How  lifestyle factors increase the risk of developing chronic disease

There is mounting evidence that slightly elevated blood glucose concentrations (even in the non-diabetic range) contribute to the development of a number of diseases including osteoarthritis. Glucose levels can influence cell behaviour and tissue health through a variety of mechanisms. In osteoarthritis, there is an increase in proteins bearing the post-translational modification O-linked N-acetylglucosamine (O-GlcNAc). Elevated glucose levels can contribute to excessive protein O-GlcNAcylation. We are interested in understanding how elevated glucose levels and aberrant protein O-GlcNAcylation contribute to disease development.     

 

We have opportunities for Summer students as well as honours, masters and PhD students.

 

 

 

 

Teaching | Current

MEDSCI 304 Molecular Pharmacology

MEDSCI 305 Systems Pharmacology

MEDSCI 700 Special Topic: Drug Discovery Biology

MEDSCI 720 Biomedical Research Techniques

MEDSCI 738 Biological Clocks

 

 

Distinctions/Honours

Sir Charles Hercus Health Research Fellowship (Health Research Council NZ) (2016).

 

Committees/Professional groups/Services