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The Molecular Mechanisms Of Anabolic Androgen Actions In Skeletal Muscle
Funder
National Health and Medical Research Council
Funding Amount
$487,500.00
Summary
We are studying the role of male sex hormones, androgens, in controlling muscle function. Muscle wasting occurs in a variety of disorders, including cancer, burns and trauma, and also during normal ageing. Treatment with androgens helps prevent muscle wasting, and causes increased muscle size, although current therapies can also have side effects. Little is known about how androgens prevent wasting and promote muscle growth. Therefore, we propose to study the actions of male sex hormones in musc ....We are studying the role of male sex hormones, androgens, in controlling muscle function. Muscle wasting occurs in a variety of disorders, including cancer, burns and trauma, and also during normal ageing. Treatment with androgens helps prevent muscle wasting, and causes increased muscle size, although current therapies can also have side effects. Little is known about how androgens prevent wasting and promote muscle growth. Therefore, we propose to study the actions of male sex hormones in muscle. We will study the growth of mouse muscle cells in culture, and measure their rate of growth when treated with androgens. All cells contain certain factors that control their growth and replication, and we will test whether androgens activate these factors to increase growth. We will also study the effect of androgens on muscle in mice, to investigate complex effects that only occur in real muscle. We will neuter male mice, which causes muscle wasting. Neutered mice will then be treated with androgens or placebo, and we will compare the muscle growth effect of androgen treatment versus placebo. We will measure muscle strength, size, and the number of muscle cells in treated and placebo mice. We will also see if the effects of androgen require a particular protein, the androgen receptor, which acts as a lock-key mechanism in cells, to allow them to respond to androgens. We will make a strain of mouse with a non-functional version of the androgen receptor only in muscle cells. This will determine if the muscle growth effects of androgens occur through a direct action on muscle, or indirectly through acting on other tissues in the body. This information will ultimately allow us to design more targeted androgen therapies for muscle wasting, that act only on muscle.Read moreRead less
Targeting Calcineurin For Improving Muscle Regeneration In Skeletal Muscle Disease
Funder
National Health and Medical Research Council
Funding Amount
$303,000.00
Summary
Muscular dystrophy is a term that covers a diverse group of inherited disorders characterised by progressive muscle weakness and wasting. Duchenne muscular dystrophy (DMD) is the most severe form, caused by a lack of a protein called dystrophin, which renders muscles fragile, susceptible to damage, and with a compromised ability to regenerate or repair after injury. The disease progresses to all muscles and DMD patients are dependent on a wheelchair before their early teens and die in their twen ....Muscular dystrophy is a term that covers a diverse group of inherited disorders characterised by progressive muscle weakness and wasting. Duchenne muscular dystrophy (DMD) is the most severe form, caused by a lack of a protein called dystrophin, which renders muscles fragile, susceptible to damage, and with a compromised ability to regenerate or repair after injury. The disease progresses to all muscles and DMD patients are dependent on a wheelchair before their early teens and die in their twenties. There is a profound need for treatments that can ameliorate the dystrophic condition and improve patient quality of life. Restoring or increasing a muscle's capacity to regenerate would help improve muscle function. We have convincing evidence that the calcineurin signal transduction pathway is important for successful muscle regeneration in mice with muscular dystrophy. There is growing excitement worldwide that stimulating calcineurin could attenuate the dystrophic pathology, however, little is known about the role of calcineurin signalling in human muscle disease. Our goals are to investigate the role of calcineurin signalling in muscular dystrophy and to examine its therapeutic potential for enhancing muscle regeneration. Our aim is to better understand the mechanisms controlling calcineurin signalling in muscles of dystrophic mice and in muscles of patients with DMD. A comprehensive series of physiological, molecular, biochemical, and immunohistochemical experiments will be performed to rigorously test our research aim. Understanding the role of the calcineurin pathway in muscle regeneration is important for the development of novel therapeutic strategies to delay the onset or slow the progression of muscle wasting and weakness. The findings will have broad clinical application for our understanding of muscular dystrophy with relevance to other conditions including ageing, AIDS, burns, cancer cachexia, and disuse atrophy, where muscle wasting occurs.Read moreRead less
A Novel Cytoskeletal Structure In Muscle Is Associated With Muscular Dystrophy
Funder
National Health and Medical Research Council
Funding Amount
$371,250.00
Summary
A NEW PROTEIN NETWORK IN MUSCLE IS ASSOCIATED WITH MUSCLE DISEASE An intricate protein network connects the contracting mechanism of a muscle to the surrounding cell membrane. Disruption of this connection is one of the known causes of muscular dystrophy. For many patients however the cause of the disease is unknown. We have identified a new region within this protein network that is also associated with muscle disease in mice. A number of proteins that are involved in transmitting chemical mess ....A NEW PROTEIN NETWORK IN MUSCLE IS ASSOCIATED WITH MUSCLE DISEASE An intricate protein network connects the contracting mechanism of a muscle to the surrounding cell membrane. Disruption of this connection is one of the known causes of muscular dystrophy. For many patients however the cause of the disease is unknown. We have identified a new region within this protein network that is also associated with muscle disease in mice. A number of proteins that are involved in transmitting chemical messages from one part of the muscle cell to another are found at this same location. It is possible that disruption of these messages may lead to muscle disease. This project aims to establish the nature of the relationship between the proteins found in this newly identified region of the protein network and muscle diseases such as muscular dystrophy, in both animal models and in humans. We expect that this project may identify new markers for identifying the cause of muscle diseases in some patients and lead to better hopes for an eventual cure.Read moreRead less
Modulating Heat Shock Protein Expression In Skeletal Muscle To Improve The Pathophysiology Of Muscular Dystrophy
Funder
National Health and Medical Research Council
Funding Amount
$502,361.00
Summary
Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy. Dystrophic muscles are fragile, prone to injury, and regenerate poorly after damage. Defective calcium handling has been implicated in these processes. We have revealed that upregulating levels of stress proteins called _heat shock proteins� (HSPs) can improve calcium regulation in muscular dystrophy. Modulating the HSP response has significant potential to delay the onset or slow the progression of DMD.
Regulatory Mechanisms And Roles Of Calpains In Skeletal Muscle
Funder
National Health and Medical Research Council
Funding Amount
$439,813.00
Summary
The objectives are to understand the regulation and roles of calpains, which are proteases that break proteins in the building and repair of skeletal muscle. We will determine targets that calpains cleave and whether their location changes following activation, as well as the cellular factors regulating their activity. In addition, we will obtain information about the specific type of calpain dysfunction that occurs in particular patients with limb girdle muscular dystrophy 2A.
Advancing The Diagnosis And Treatment Of Inherited Muscle Disorders
Funder
National Health and Medical Research Council
Funding Amount
$408,388.00
Summary
Inherited myopathies collectively affect ~1 in 1000 people, cause life-long disability and often shortened life. This fellowship addresses two key areas of need. 1. New gene discovery for the inherited myopathies using the latest genetic techniques and 2. developing therapies. I will test two recently developed drugs as potential treatments for tropomyosin myopathies and investigate key areas of disease mechanism for tropomyosin and RYR1 myopathies to identify new therapeutic targets.
Understanding The Cause Of Muscle Weakness In Nemaline Myopathy (NM) – Moving Towards The Development Of Targeted Treatments
Funder
National Health and Medical Research Council
Funding Amount
$408,768.00
Summary
Congenital myopathy patients have unremitting, life-long muscle weakness that severely affects their quality of life and ability to perform normal daily activities. Currently no effective therapies exist for these conditions, largely due to our limited understanding of the mechanisms leading to muscle weakness. This ECF aims to determine the cause of weakness and test two therapies which have shown promise for other conditions and can be translated into clinical use for myopathies if effective.
Nerve And Muscle Excitability In Inclusion Body Myositis
Funder
National Health and Medical Research Council
Funding Amount
$81,294.00
Summary
Our study will use recently developed neurophysiological techniques to study nerve and muscle excitability in sporadic inclusion body myositis, a poorly understood progressive muscle disease for which no effective treatment is known. We will determine whether the electrical properties of nerve and muscle cell membranes are affected and obtain clues as to where this dysfunction may occur. This may aid development of effective therapies through a better understanding of disease mechanisms.