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Determining The Influences Of Cell Stress And Heat Shock Factor-1 Action In Osteoclast Formation And Pathological Bone Loss.
Funder
National Health and Medical Research Council
Funding Amount
$657,287.00
Summary
Cancer and rheumatoid arthritis cause painful bone destruction. This occurs due to increased numbers of bone destroying cells called osteoclasts. We found stress responses in bone cells can increase osteoclast numbers by activating proteins inside the bone cells that encourage osteoclasts to form. We will thus study whether cell stress blocking drugs might stop bone loss. As arthritis and cancer both cause stress responses, this work could identify a new way that such diseases affect bone.
Sclerostin: A Key Regulator Of Bone Mineralisation And Bone Catabolism
Funder
National Health and Medical Research Council
Funding Amount
$536,653.00
Summary
The regulation of bone mass is critical for many areas of human disease including osteoporosis, osteoarthritis, inflammatory bone loss conditions, e.g. rheumatoid arthritis, cancers of bone and problems relating to orthopaedic prosthesis failure. The osteocyte, the most abundant bone cell, plays a central role in normal bone biology and is likely key to these diseases. Sclerostin is one osteocyte product that may be a key to understanding how boneÍs mass and composition is controlled locally.
Novel Strategies For The Treatment Of Bone Disease By Nutrient Activators Of Calcium-sensing Receptors
Funder
National Health and Medical Research Council
Funding Amount
$467,432.00
Summary
Osteoporosis is a major health problem in the Australian community and will worsen with an ageing population. This work aims to develop new strategies for the treatment of osteoporosis and associated fractures based on the nutritional and/or pharmacological activation of calcium-sensing receptors.
Tyrosine Kinase Receptor C-ros-oncogene 1 Mediates Twist-1 Haploinsufficiency Induced Craniosynostosis In Children: A Novel Therapeutic Target
Funder
National Health and Medical Research Council
Funding Amount
$562,863.00
Summary
Children with Saethre-Chotzen syndrome exhibit premature fussed coronal sutures, and other skull/ skeletal malformations. Surgical intervention is the only treatment option to ensure optimal cognitive and skeletal development. Our studies have identified a candidate molecular pathway that regulates bone formation by cranial bone cells from these patients. Targeting these key molecular signalling components with chemical inhibitors will help prevent the premature fusion of cranial sutures.
The Role Of EphrinB1 Reverse Signalling In Osteogenic Differentiation During Skeletal Development And Osteoporosis
Funder
National Health and Medical Research Council
Funding Amount
$567,292.00
Summary
The present proposal will identify the importance of ephrinB1 during the deregulation of bone remodelling that occurs in osteoporosis, by deleting ephrinB1 in committed osteoblast precursor cells in a mouse model of osteoporosis. Knowledge gained from this proposal could potentially translate into alternative therapeutic treatment strategies for patients with osteoporosis with the use of Eph/ephrin targeted drugs currently being developed for cancer treatment.
Identifying The Physiological Actions Of Calcitonin
Funder
National Health and Medical Research Council
Funding Amount
$683,040.00
Summary
Calcitonin is a hormone whose main action has long been regarded as the slowing down of bone breakdown, however, its importance in human physiology is unknown. The aim of this study is to understand the role of calcitonin in regulating bone formation and protecting the skeleton in times of calcium stress, such as lactation. These results will greatly advance our understanding of the control of bone and calcium homeostasis, which will have implications for the treatment of bone disorders.
The Effect Of Histone Deacetylase Inhibitors On The Bone Environment In Multiple Myeloma
Funder
National Health and Medical Research Council
Funding Amount
$356,899.00
Summary
Multiple myeloma (MM) is an incurable hematological malignancy with 1,400 people diagnosed each year. Severe bone loss occurs in up to 90% of these patientssignificantly impacting on quality of life resulting in severe bone pain and bone lesions that fail to heal. This project proposes that a novel histone deacetylase inhibitor could provide an appropriate therapeutic strategy that inhibits tumor growth and prevents bone loss whilst also promoting bone repair.
The Role Of Osteocytes In Particle Induced Osteolysis
Funder
National Health and Medical Research Council
Funding Amount
$457,196.00
Summary
Hip replacements often fail due to the loss of adjacent bone. Metal or polyethylene particles are produced as the prosthesis bearing surface wears but how do these particles lead to bone loss? Our work suggests involvement of osteocytes within the bone mineral, which are increasingly understood to drive bone physiology and pathology. We will explore the role of the osteocytes by examining their response to particles, which may identify a new target to prevent particle-induced bone loss.
Targeting Bone Marrow Lesions To Find Interventions In The Progression Of Osteoarthritis
Funder
National Health and Medical Research Council
Funding Amount
$467,395.00
Summary
It is essential to elucidate the underlying cause(s) of osteoarthritis because our current level of understanding of this condition has failed to produce effective treatments. Lesions in the bone under the cartilage (BMLs), seen using MRI, have strong potential value for the objective monitoring and management of OA. However, because the nature of BMLs is not well understood, the aim of this application is to perform a comprehensive study of BMLs in OA bone.
Novel Treatment Approaches To Prevent Joint Fusion In Ankylosing Spondylitis
Funder
National Health and Medical Research Council
Funding Amount
$477,440.00
Summary
Ankylosing spondylitis (AS) is a form of arthritis targeting the spine and pelvis that causes uncontrolled bone formation resulting in complete joint fusion, severe disability and even death for which no therapies are currently available. Using a mouse model that closely replicates the human disease we will characterise the changes causing this joint fusion and identify possible new targets to develop novel treatments.