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The Role Of The Human RECK Protein In Modifying Human Sarcoma Progression Within In Vitro And In Vivo Models
Funder
National Health and Medical Research Council
Funding Amount
$34,878.00
Summary
The protein “RECK” is known to have a controlling effect on cancers by reducing growth, invasion, and blood supply. RECK is present in normal tissues but in bone and soft-tissue tumours (sarcomas), the protein is reduced. This study aims to; correlate RECK levels in sarcoma with patient survival, use gene technology to increase RECK levels in sarcoma cells, and observe the effects on sarcoma invasion and metastasis.
Detecting Bioactivity In A Naturally-occurring Aggrecan Fragment
Funder
National Health and Medical Research Council
Funding Amount
$407,634.00
Summary
The dynamic balance of anabolic and catabolic processes in healthy cartilage is disturbed in arthritis, with increased catabolism leading to irreparable cartilage damage. We will study the ability of a naturally-occuring aggrecan fragment to modulate cartilage catabolism. Our in vitro and in vivo experiments suggest that the aggrecan fragment limits cartilage destruction. This study tests our hypothesis that the aggrecan fragment antagonises cartilage damage and promote cartilage repair.
Novel Pathways Involving APC And PAR-2 In Cartilage Degradation In Osteoarthritis
Funder
National Health and Medical Research Council
Funding Amount
$448,834.00
Summary
Loss of the cartilage that normally lines the ends of bones is central to joint failure in arthritis and the need for replacement surgery. There are presently no treatments that stop cartilage breakdown in joint disease. This project investigates the role of a new pathway not previously thought to be active in cartilage, in the progressive damage seen in arthritis. Successful completion of these studies may provide a novel new strategy to treat joint disease.
Improving Muscular Dystrophy By Targeting The ADAMTS5 Metalloproteinase
Funder
National Health and Medical Research Council
Funding Amount
$658,571.00
Summary
Muscular dystrophy is a devastating childhood disorder. There is no cure and no effective therapy to stop the disease progressing to early death. Our pilot data show that muscular dystrophy in a mouse model is dramatically improved when the Adamts5 gene is inactivated. ADAMTS5 is an enzyme that remodels the extracellular matrix around cells. This suggests that inhibiting ADAMTS5 may be a new way to treat muscular dystrophy. We will test this idea in mice with muscular dystrophy
INVESTIGATIONS ON THE REGULATION OF INTERVERTEBRAL DISC CELL MATRIX METALLOPROTEINASES
Funder
National Health and Medical Research Council
Funding Amount
$331,320.00
Summary
Degeneration of the intervertebral disc is a painful disabling condition with major socioeconomic consequences. Medical problems associated with disc degeneration and back-pain, of sufficient severity to warrant consultation with a physician, are experienced by 90% of the population some time during their lives. In man, back pain increases in incidence in the third and fourth decades of life, peaks in the fifties and declines thereafter. Changes in population demographics indicate this problem w ....Degeneration of the intervertebral disc is a painful disabling condition with major socioeconomic consequences. Medical problems associated with disc degeneration and back-pain, of sufficient severity to warrant consultation with a physician, are experienced by 90% of the population some time during their lives. In man, back pain increases in incidence in the third and fourth decades of life, peaks in the fifties and declines thereafter. Changes in population demographics indicate this problem will increase in severity over the next few decades. American Bureau of Census data indicate that between 1990 to 2010 the number of people >45 years will increase from 82 to 124 million, the number of elderly in emerging countries will also increase between 200 to 400% in the next 30 years. In the United States, back-pain is the second most common reason that people visit a physician and medical conditions related to back-pain account for more hospitalisations than any other musculoskeletal disorder. Despite its high incidence, associated problems of incapacity and economic implications, costed at $100 million per annum in Australia in 1992, and US$100 billion globally in 1999-2000 (Dorland Data Networks, PA, USA) the causes of low back-pain are still poorly understood. Disc disease is responsible for 23-40% of all cases of low back-pain. The management of discogenic low back-pain is currently empirical, directed either toward life-style changes to minimise symptomatology or to surgical resection or spinal arthrodesis to restrict articulation. Based on our recent findings and those of colleagues over the last 16 years, it is our strong conviction that it should be possible with a better understanding of disease mechanisms and with the use of modern technologies to inhibit, reverse or ideally prevent disc degeneration. Without such basic research there will be no scientific foundation upon which prospective therapies may be based.Read moreRead less
Chondrocyte Hypertrophy In Development And Disease
Funder
National Health and Medical Research Council
Funding Amount
$360,018.00
Summary
Whereas chondrocyte hypertrophy is a normal feature of skeletal growth, in adult chondrocytes it is associated with osteoarthritis (OA). We propose that collagen II fragments provide signals for hypertrophy in cartilage. The lack of collagen II fragments in our collagenase-resistant mouse provides a unique opportunity to address the role of collagen II fragments in driving cellular hypertrophy. We will identify bioactive collagen II fragments that represent novel targets for OA therapies
Preventing Kidney Fibrosis By Targeting Matrix Metalloproteinase-9 In Chronic Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$516,972.00
Summary
More than 2300 Australians commence kidney replacement therapy each year and many more die of kidney failure or its complications. Kidney fibrosis is the final pathway of damage in all chronic kidney diseases. Our data demonstrates that a matrix enzyme MMP-9 is likely to be an important cause of kidney fibrosis. We aim to investigate mechanisms by which MMP-9 causes kidney fibrosis, and develop strategies involving inhibition of MMP-9 to prevent kidney fibrosis.
Development And Pre-clinical Evaluation Of A Novel Wound Dressing Treatment For Chronic Ulcers
Funder
National Health and Medical Research Council
Funding Amount
$125,040.00
Summary
Chronic leg ulcers are a common, painful and costly reality for many Australians, impacting on sufferers' mobility, social interactions and overall quality of life. This research is directed at developing a novel cost-effective wound dressing for treatment of this condition. This will be achieved through neutralising the ulcer's toxic proteolytic environment through an interactive wound dressing. This then will allow the body's own cells to promote wound healing.
To Understand The Role Of The Plasminogen Activating And Matrix Metalloproteinase Systems In Traumatic Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$499,321.00
Summary
Tissue-type plasminogen activator (t-PA) is known for its role as a clot dissolving protein. It is present in the brain and following traumatic brain injury (TBI), it can worse brain cell damage. We have established a mouse model of TBI . We will compare brain damage in mice that are deficient in or have high amounts of t-PA. We will also determine whether the recovery rate post-TBI can be improved using specific t-PA blockers. This project may provide new therapies for TBI.