Dr Raewyn Carol Poulsen
BSc (Biochemistry), MScHons (First Class), PhD (Biochemistry)
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
Sir Charles Hercus Health Research Fellowship (Health Research Council NZ) (2016).
Selected publications and creative works (Research Outputs)
- Rong, J., Pool, B., Zhu, M., Munro, J., Cornish, J., McCarthy, G. M., ... Poulsen, R. (2019). Basic Calcium Phosphate Crystals Induce Osteoarthritis-Associated Changes in Phenotype Markers in Primary Human Chondrocytes by a Calcium/Calmodulin Kinase 2-Dependent Mechanism. Calcified tissue international, 104 (3), 331-343. 10.1007/s00223-018-0494-1
Other University of Auckland co-authors: Jillian Cornish, Nicola Dalbeth, Jing Rong, Jacob Munro
- Rong, J., Zhu, M., Munro, J., Cornish, J., McCarthy, G. M., Dalbeth, N., & Poulsen, R. C. (2019). Altered expression of the core circadian clock component PERIOD2 contributes to osteoarthritis-like changes in chondrocyte activity. Chronobiology international, 36 (3), 319-331. 10.1080/07420528.2018.1540493
Other University of Auckland co-authors: Jing Rong, Jacob Munro, Jillian Cornish, Nicola Dalbeth
- Kalev-Zylinska, M. L., Hearn, J. I., Rong, J., Zhu, M., Munro, J., Cornish, J., ... Poulsen, R. C. (2018). Altered N-methyl D-aspartate receptor subunit expression causes changes to the circadian clock and cell phenotype in osteoarthritic chondrocytes. Osteoarthritis and cartilage, 26 (11), 1518-1530. 10.1016/j.joca.2018.06.015
Other University of Auckland co-authors: Maggie Kalev, James Hearn, Jing Rong, Mark Zhu, Jacob Munro, Jillian Cornish, Nicola Dalbeth
- Poulsen, R. C., Warman, G. R., Sleigh, J., Ludin, N. M., & Cheeseman, J. F. (2018). How does general anaesthesia affect the circadian clock?. Sleep Medicine Reviews, 37, 35-44. 10.1016/j.smrv.2016.12.002
Other University of Auckland co-authors: James Cheeseman, Guy Warman, Nicola Ludin, Jamie Sleigh
- Snelling, S. J. B., Forster, A., Mukherjee, S., Price, A. J., & Poulsen, R. C. (2016). The chondrocyte-intrinsic circadian clock is disrupted in human osteoarthritis. Chronobiology International: the journal of biological and medical rhythm research, 33 (5), 574-579. 10.3109/07420528.2016.1158183
- Poulsen, R. C., Carr, A. J., & Hulley, P. A. (2015). Cell proliferation is a key determinant of the outcome of FOXO3a activation. Biochemical and Biophysical Research Communications, 462 (1), 78-84. 10.1016/j.bbrc.2015.04.112
- Poulsen, R. C., Watts, A. C., Murphy, R. J., Snelling, S. J., Carr, A. J., & Hulley, P. A. (2014). Glucocorticoids induce senescence in primary human tenocytes by inhibition of sirtuin 1 and activation of the p53/p21 pathway: in vivo and in vitro evidence. Annals of the Rheumatic Diseases, 73 (7), 1405-1413. 10.1136/annrheumdis-2012-203146
- Poulsen, R. C., Knowles, H. J., Carr, A. J., & Hulley, P. A. (2014). Cell differentiation versus cell death: extracellular glucose is a key determinant of cell fate following oxidative stress exposure. Cell Death and Disease, 510.1038/cddis.2014.52