Furin: Carving-up Vital Substrates For Bone Remodelling And Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$815,972.00
Summary
Osteoporosis, or porous bone, is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures. It is caused by an imbalance between the cells that are constantly reabsorbing and reforming bone. The proposed project will address furin as a novel regulator of bone remodelling.
Myo1b Bridges The Actin-membrane Interface During Osteoclastic Bone Resorption
Funder
National Health and Medical Research Council
Funding Amount
$429,387.00
Summary
Osteoporosis is a debilitating bone disease which features progressive bone loss. Bone loss (resorption) is driven by the bone resident cell the osteoclast. Identifying molecules that regulate bone resorption by osteoclasts is a crucial first step towards developing new targets for theraputic intervention. This proposal explores the role of Myo1b, a novel protein that appears to facilitate osteoclastic bone resorption and thus represents an attractive new candidate to target bone loss.
The Role Of CHKB In Osteoclastic Bone Resorption And Bone Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$565,695.00
Summary
Osteoporosis is a devastating disorder. Osteoporotic fractures in the elderly have been correlated with increased mortality rates. Osteoporosis alone costs $13.8 billion p.a. in USA and tens of millions of dollars in Australia. Cost to society of our ageing population for people become disabled by hip fractures alone could triple by the year 2040. Our research examines the role of CHKB in bone loss which may underscore its potential as a new molecular target for anti-resorptive drug development.
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.
Control Of Bone Remodelling By Osteoclastic Metabolism Of Vitamin D
Funder
National Health and Medical Research Council
Funding Amount
$694,635.00
Summary
Vitamin D is essential for bone health. This study will build on our extensive body of preliminary data to investigate the extent to which bone-resorbing osteoclasts are controlled by circulating levels of the pro-hormone 25-hydroxyvitamin D. Our work will identify new approaches to the treatment of osteoporosis, by targetting the osteoclast as a vitamin D-responsive cell type.
Monitoring Bone Loss And Response To Therapy Through Bone Material And Structural Composition
Funder
National Health and Medical Research Council
Funding Amount
$696,111.00
Summary
Millions of scripts are filled for treatment of osteoporosis. However, there is no way of knowing if these drugs are right for these individuals, if it improves bone strength or are actually doing harm. Bone density measurement is of limited value. We have developed a new analysis method that measures changes in bone structure that tell us if the treatment is or is not working so alternative treatment can be used. The aim of this study is to test this new method.
Identification Of Novel PTH Anabolic Targets In Osteoblasts
Funder
National Health and Medical Research Council
Funding Amount
$547,216.00
Summary
Osteoporosis is a major disease affecting Australians. Whilst there are a number of drugs available that will reduce bone loss, there are few drugs available that build new bone, and little is known of the action of these drugs. New targets have been identified that modulate bone formation, and this project aims to validate these in appropriate models and determine their mechanism of action.
Optimising Bone Regeneration Using Advanced Design And Fabrication Technologies
Funder
National Health and Medical Research Council
Funding Amount
$916,671.00
Summary
The aging population has produced a rapidly increasing demand for synthetic implants that can regenerate lost or diseased bone. This project will produce an implant that represents a viable alternative to bone autografts and allografts with broad applications for the repair of large or challenging bone defects. Such an achievement will have significant healthcare benefits by reducing patient morbidity and recovery time, and improving long-term outcomes.
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 boneĆs mass and composition is controlled locally.