Prince Henry’s Institute

 

Julian Quinn

 

Profile

Dr Quinn began his career at the University of Oxford where he completed doctoral and post-doctoral studies on bone biology and subsequently continued this work at the University of Melbourne.

For over 12 years he was a research fellow at St Vincent's Institute in Melbourne where he worked with Professors Matthew Gillespie and Jack Martin on a range of basic research programs investigating bone physiology.

He joined PHI in June 2008.

 

Research Interests

Dr Quinn has worked since 1985 on the characterisation of the cells of bone and how they work together to regulate and renew the bone.

He has had a particular interest in the osteoclast, a type of cell uniquely specialised to break down bone using a mixture of acid and destructive enzymes. Dr Quinn has made significant contributions to both the characterisation of this cell and to the understanding of how osteoclast formation is controlled, and originally developed.

He is currently investigating how bone is normally remodelled and renewed under as it ages, but also has a strong interest in how osteoclasts cause the bone destruction that is seen in a range of diseases that affect bone. These include common diseases such as joint inflammation (e.g. arthritis) and tumour invasion, as well as metabolic diseases such as osteoporosis.

The bone destruction that accompanies such diseases result in debilitating pain and fractures constitute a major and worsening health problem, particularly in elderly people to whom fractures can be life threatening.

Areas of special interest:

• The formation and activation of osteoclast cells.

• Determining how the immune system influences bone loss, and particularly the role that lymphocytes play in blocking osteoclast formation.

• Investigating how drug-induced stress responses may make bone loss worse, particularly in cancer patients.

• Studying how osteoclasts interact with bone building cells. Bone removal by osteoclasts normally triggers new bone formation to balance the bone loss. It is not understood how this stimulation is controlled, but it becomes defective or ineffective in advanced age and with certain drug treatments, resulting in insufficient new bone.

 

Current Research

• Prevention of bone loss

• Factors affecting osteoblast differentiation

 

Recent Achievements

• Determined that lymphocytes are able to mediate the actions of immune cytokines (including IL-23 and IL-33) which can block osteoclast formation.

• Demonstrated that a number of drugs under development for cancer and diabetes accelerate osteoclast formation and cause bone loss in rodent models.

 

Service to Scientific Community

• Editorial Board - BONE (since 2007)

 

Selected Publications

Quinn JMW, Saleh H. (2009) Modulation of Osteoclast Function in Bone by the Immune System. Mol Cell Endocrinol (in press)

Quinn JMW, Sims NA, Saleh H, Mirosa D, Thompson K, Bouralexis S, Walker EC, Martin TJ and Gillespie MT. (2008). Interleukin-23 inhibits osteoclastogenesis indirectly through lymphocytes and is required for the maintenance of bone mass in mice. J Immunol 181:5720-9.

Nakamura A, Ly C, Sims NA, Kartsogiannis V, Bouralexis S, Saleh H, Zhou H, Martin TJ, Ng KW, Gillespie MT, Quinn JMW. (2007) Osteoclast inhibitory lectin (OCIL) inhibits osteoblast differentiation and functionin vitro.  Bone 40:305-315.

Martin TJ, Quinn JMW, Gillespie MT, Ng KW, Karsdal MA, Sims NA. (2006) Mechanisms involved in skeletal anabolic therapies. Ann NY Acad Sci 1068:458-470.

Quinn JMW, Gillespie MT. (2005) Modulators of osteoclast formation. Biochem Biophys Res Commun 328:739-745.

Sims NA, Jenkins BJ, Nakamura A, Quinn JMW, Li R, Gillespie MT, Ernst M, Robb L, Martin TJ. (2005) Interleukin-11 receptor signaling is required for normal bone remodeling. J Bone Mineral Res 20:1093-1102. 

Price JT*, Quinn JMW*, Sims NA, Vieusseux J, Waldeck K, Docherty SE, Myers DM, Nakamura A, Waltham MC, Gillespie MT, Thompson EW. (2005)  The heat shock protein 90 inhibitor, 17-Allylamino-17-desmethoxygeldanamycin, enhances osteoclast formation and potentiates bone metastasis in a human breast cancer cell line model. Cancer Res 65:4929-4938. *Joint first authors.